Reference Citation Analysis: Find an Article, Find a Category, Find a Journal, Find a Scholar

For: Huber N, Sakai N, Eismann T, Shin T, Kuboki S, Blanchard J, Schuster R, Edwards MJ, Wong HR, Lentsch AB. Age-related decrease in proteasome expression contributes to defective nuclear factor-kappaB activation during hepatic ischemia/reperfusion. Hepatology 2009;49:1718-28. [PMID: 19206148 PMCID: PMC2695826 DOI: 10.1002/hep.22840] [Citation(s) in RCA: 36] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/18/2023]

For:	Huber N, Sakai N, Eismann T, Shin T, Kuboki S, Blanchard J, Schuster R, Edwards MJ, Wong HR, Lentsch AB. Age-related decrease in proteasome expression contributes to defective nuclear factor-kappaB activation during hepatic ischemia/reperfusion. Hepatology 2009;49:1718-28. [PMID: 19206148 PMCID: PMC2695826 DOI: 10.1002/hep.22840] [Citation(s) in RCA: 36] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/18/2023]

Number

Cited by Other Article(s)

Liu Z, Xu J, Que T, Que S, Valenti L, Zheng S. Molecular Mechanisms of Ischemia/Reperfusion Injury and Graft Dysfunction in Liver Transplantation: Insights from Multi-Omics Studies in Rodent Animal Models. Int J Biol Sci 2025;21:2135-2154. [PMID: 40083684 PMCID: PMC11900806 DOI: 10.7150/ijbs.109449] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/26/2024] [Accepted: 01/25/2025] [Indexed: 03/16/2025] Open

Affiliation(s)

Zhengtao Liu Key Laboratory of Artificial Organs and Computational Medicine in Zhejiang Province, Shulan International Medical College, Zhejiang Shuren University, Hangzhou, China Shulan Hospital (Hangzhou), Hangzhou, China NHC Key Laboratory of Combined Multi-Organ Transplantation, Key Laboratory of the Diagnosis and Treatment of Organ Transplantation, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China Key Laboratory of Organ Transplantation, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
Jun Xu NHC Key Laboratory of Combined Multi-Organ Transplantation, Key Laboratory of the Diagnosis and Treatment of Organ Transplantation, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China Key Laboratory of Organ Transplantation, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China Division of Hepatobiliary and Pancreatic Surgery, Department of Surgery, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
Ting Que Birth Defects Prevention and Control Institute, Maternal and Child Health Hospital of Guangxi Zhuang Autonomous Region, Nanning, China
Shuping Que DingXiang Clinics, Hangzhou, China
Luca Valenti Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy Precision Medicine, Biological Resource Center Unit, Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Milan, Italy
Shusen Zheng Key Laboratory of Artificial Organs and Computational Medicine in Zhejiang Province, Shulan International Medical College, Zhejiang Shuren University, Hangzhou, China Shulan Hospital (Hangzhou), Hangzhou, China NHC Key Laboratory of Combined Multi-Organ Transplantation, Key Laboratory of the Diagnosis and Treatment of Organ Transplantation, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China Key Laboratory of Organ Transplantation, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China Division of Hepatobiliary and Pancreatic Surgery, Department of Surgery, First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China

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Zhang M, Liu Q, Meng H, Duan H, Liu X, Wu J, Gao F, Wang S, Tan R, Yuan J. Ischemia-reperfusion injury: molecular mechanisms and therapeutic targets. Signal Transduct Target Ther 2024;9:12. [PMID: 38185705 PMCID: PMC10772178 DOI: 10.1038/s41392-023-01688-x] [Citation(s) in RCA: 114] [Impact Index Per Article: 114.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/29/2023] [Revised: 08/29/2023] [Accepted: 10/18/2023] [Indexed: 01/09/2024] Open

Abstract

Ischemia-reperfusion (I/R) injury paradoxically occurs during reperfusion following ischemia, exacerbating the initial tissue damage. The limited understanding of the intricate mechanisms underlying I/R injury hinders the development of effective therapeutic interventions. The Wnt signaling pathway exhibits extensive crosstalk with various other pathways, forming a network system of signaling pathways involved in I/R injury. This review article elucidates the underlying mechanisms involved in Wnt signaling, as well as the complex interplay between Wnt and other pathways, including Notch, phosphatidylinositol 3-kinase/protein kinase B, transforming growth factor-β, nuclear factor kappa, bone morphogenetic protein, N-methyl-D-aspartic acid receptor-Ca2+-Activin A, Hippo-Yes-associated protein, toll-like receptor 4/toll-interleukine-1 receptor domain-containing adapter-inducing interferon-β, and hepatocyte growth factor/mesenchymal-epithelial transition factor. In particular, we delve into their respective contributions to key pathological processes, including apoptosis, the inflammatory response, oxidative stress, extracellular matrix remodeling, angiogenesis, cell hypertrophy, fibrosis, ferroptosis, neurogenesis, and blood-brain barrier damage during I/R injury. Our comprehensive analysis of the mechanisms involved in Wnt signaling during I/R reveals that activation of the canonical Wnt pathway promotes organ recovery, while activation of the non-canonical Wnt pathways exacerbates injury. Moreover, we explore novel therapeutic approaches based on these mechanistic findings, incorporating evidence from animal experiments, current standards, and clinical trials. The objective of this review is to provide deeper insights into the roles of Wnt and its crosstalk signaling pathways in I/R-mediated processes and organ dysfunction, to facilitate the development of innovative therapeutic agents for I/R injury.

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Meng F, Zhou Y, Wagner A, Bülow JM, Köhler K, Neunaber C, Bundkirchen K, Relja B. Impact of age on liver damage, inflammation, and molecular signaling pathways in response to femoral fracture and hemorrhage. Front Immunol 2023;14:1239145. [PMID: 37691959 PMCID: PMC10484338 DOI: 10.3389/fimmu.2023.1239145] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/12/2023] [Accepted: 08/07/2023] [Indexed: 09/12/2023] Open

Abstract

Background

Trauma causes disability and mortality globally, leading to fractures and hemorrhagic shock. This can trigger an irregular inflammatory response that damages remote organs, including liver. Aging increases the susceptibility to dysregulated immune responses following trauma, raising the risk of organ damage, infections, and higher morbidity and mortality in elderly patients. This study investigates how aging affects liver inflammation and damage post-trauma.

Methods

24 male C57BL/6J mice were randomly divided into four groups. Twelve young (17-26 weeks) and 12 aged (64-72 weeks) mice were included. Mice further underwent either hemorrhagic shock (trauma/hemorrhage, TH), and femoral fracture (osteotomy) with external fixation (Fx) (THFx, n=6) or sham procedures (n=6). After 24 hours, mice were sacrificed. Liver injury and apoptosis were evaluated using hematoxylin-eosin staining and activated caspase-3 immunostaining. CXCL1 and infiltrating polymorphonuclear leukocytes (PMNL) in the liver were assessed by immunostaining, and concentrations of CXCL1, TNF, IL-1β, and IL-10 in the liver tissue were determined by ELISA. Gene expression of Tnf, Cxcl1, Il-1β, and Cxcl2 in the liver tissue was determined by qRT-PCR. Finally, western blot was used to determine protein expression levels of IκBα, Akt, and their phosphorylated forms.

Results

THFx caused liver damage and increased presence of active caspase-3-positive cells compared to the corresponding sham group. THFx aged group had more severe liver injury than the young group. CXCL1 and PMNL levels were significantly higher in both aged groups, and THFx caused a greater increase in CXCL and PMNL levels in aged compared to the young group. Pro-inflammatory TNF and IL-1β levels were elevated in aged groups, further intensified by THFx. Anti-inflammatory IL-10 levels were lower in aged groups. Tnf and Cxcl1 gene expression was enhanced in the aged sham group. Phosphorylation ratio of IκBα was significantly increased in the aged sham group versus young sham group. THFx-induced IκBα phosphorylation in the young group was significantly reduced in the aged THFx group. Akt phosphorylation was significantly reduced in the THFx aged group compared to the THFx young group.

Conclusion

The findings indicate that aging may lead to increased vulnerability to liver injury and inflammation following trauma due to dysregulated immune responses.

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Kang D, Baek Y, Lee JS. Mechanisms of RNA and Protein Quality Control and Their Roles in Cellular Senescence and Age-Related Diseases. Cells 2022;11:cells11244062. [PMID: 36552825 PMCID: PMC9777292 DOI: 10.3390/cells11244062] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/10/2022] [Revised: 12/04/2022] [Accepted: 12/13/2022] [Indexed: 12/23/2022] Open

Wu J, Yu C, Zeng X, Xu Y, Sun C. Protection of propofol on liver ischemia reperfusion injury by regulating Cyp2b10/ Cyp3a25 pathway. Tissue Cell 2022;78:101891. [DOI: 10.1016/j.tice.2022.101891] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/01/2022] [Revised: 07/09/2022] [Accepted: 08/05/2022] [Indexed: 11/25/2022]

Hsp90-associated DNA replication checkpoint protein and proteasome-subunit components are involved in the age-related macular degeneration. Chin Med J (Engl) 2021;134:2322-2332. [PMID: 34629418 PMCID: PMC8510006 DOI: 10.1097/cm9.0000000000001773] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/10/2023] Open

Abstract

Background:

Age-related macular degeneration (AMD) is the leading cause of vision loss worldwide. However, the mechanisms involved in the development and progression of AMD are poorly delineated. We aimed to explore the critical genes involved in the progression of AMD.

Methods:

The differentially expressed genes (DEGs) in AMD retinal pigment epithelial (RPE)/choroid tissues were identified using the microarray datasets GSE99248 and GSE125564, which were downloaded from the gene expression omnibus database. The overlapping DEGs from the two datasets were screened to identify DEG-related biological pathways using gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. The hub genes were identified from these DEGs through protein-protein interaction network analyses. The expression levels of hub genes were evaluated by quantitative real-time polymerase chain reaction following the induction of senescence in ARPE-19 with FK866. Following the identification of AMD-related key genes, the potential small molecule compounds targeting the key genes were predicted by PharmacoDB. Finally, a microRNA-gene interaction network was constructed.

Results:

Microarray analyses identified 174 DEGs in the AMD RPE compared to the healthy RPE samples. These DEGs were primarily enriched in the pathways involved in the regulation of DNA replication, cell cycle, and proteasome-mediated protein polyubiquitination. Among the top ten hub genes, HSP90AA1, CHEK1, PSMA4, PSMD4, and PSMD8 were upregulated in the senescent ARPE-19 cells. Additionally, the drugs targeting HSP90AA1, CHEK1, and PSMA4 were identified. We hypothesize that Hsa-miR-16-5p might target four out of the five key DEGs in the AMD RPE.

Conclusions:

Based on our findings, HSP90AA1 is likely to be a central gene controlling the DNA replication and proteasome-mediated polyubiquitination during the RPE senescence observed in the progression of AMD. Targeting HSP90AA1, CHEK1, PSMA4, PSMD4, and/or PSMD8 genes through specific miRNAs or small molecules might potentially alleviate the progression of AMD through attenuating RPE senescence.

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1,4-dihydropyridine derivatives increase mRNA expression of Psma3, Psmb5, and Psmc6 in rats. ACTA ACUST UNITED AC 2021;72:148-156. [PMID: 34187104 PMCID: PMC8265202 DOI: 10.2478/aiht-2021-72-3422] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/01/2020] [Accepted: 06/01/2021] [Indexed: 11/21/2022]

Fagenson AM, Xu K, Saaoud F, Nanayakkara G, Jhala NC, Liu L, Drummer C, Sun Y, Lau KN, Di Carlo A, Jiang X, Wang H, Karhadkar SS, Yang X. Liver Ischemia Reperfusion Injury, Enhanced by Trained Immunity, Is Attenuated in Caspase 1/Caspase 11 Double Gene Knockout Mice. Pathogens 2020;9:pathogens9110879. [PMID: 33114395 PMCID: PMC7692674 DOI: 10.3390/pathogens9110879] [Citation(s) in RCA: 33] [Impact Index Per Article: 6.6] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/12/2020] [Revised: 10/17/2020] [Accepted: 10/20/2020] [Indexed: 12/14/2022] Open

Affiliation(s)

Alexander M. Fagenson Department of Surgery, Division of Abdominal Organ Transplant, Lewis Katz School of Medicine, Temple University, 3401 N. Broad Street, Philadelphia, PA 19140, USA; (K.N.L.); (A.D.C.); (S.S.K.) Centers for Cardiovascular Research, Inflammation, Translational and Clinical Lung Research, Metabolic Disease Research, Thrombosis Research, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA; (K.X.); (F.S.); (G.N.); (C.D.); (Y.S.); (X.J.) Correspondence: (A.M.F.); (X.Y.)
Keman Xu Centers for Cardiovascular Research, Inflammation, Translational and Clinical Lung Research, Metabolic Disease Research, Thrombosis Research, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA; (K.X.); (F.S.); (G.N.); (C.D.); (Y.S.); (X.J.) Centers for Metabolic Disease Research, Cardiovascular Research and Thrombosis Research, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA; (L.L.); (H.W.)
Fatma Saaoud Centers for Cardiovascular Research, Inflammation, Translational and Clinical Lung Research, Metabolic Disease Research, Thrombosis Research, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA; (K.X.); (F.S.); (G.N.); (C.D.); (Y.S.); (X.J.)
Gayani Nanayakkara Centers for Cardiovascular Research, Inflammation, Translational and Clinical Lung Research, Metabolic Disease Research, Thrombosis Research, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA; (K.X.); (F.S.); (G.N.); (C.D.); (Y.S.); (X.J.) Eccles Institute of Human Genetics, University of Utah, Salt Lake City, UT 84112, USA
Nirag C. Jhala Department of Pathology and Laboratory Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA;
Lu Liu Centers for Metabolic Disease Research, Cardiovascular Research and Thrombosis Research, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA; (L.L.); (H.W.)
Charles Drummer Centers for Cardiovascular Research, Inflammation, Translational and Clinical Lung Research, Metabolic Disease Research, Thrombosis Research, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA; (K.X.); (F.S.); (G.N.); (C.D.); (Y.S.); (X.J.)
Yu Sun Centers for Cardiovascular Research, Inflammation, Translational and Clinical Lung Research, Metabolic Disease Research, Thrombosis Research, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA; (K.X.); (F.S.); (G.N.); (C.D.); (Y.S.); (X.J.)
Kwan N. Lau Department of Surgery, Division of Abdominal Organ Transplant, Lewis Katz School of Medicine, Temple University, 3401 N. Broad Street, Philadelphia, PA 19140, USA; (K.N.L.); (A.D.C.); (S.S.K.)
Antonio Di Carlo Department of Surgery, Division of Abdominal Organ Transplant, Lewis Katz School of Medicine, Temple University, 3401 N. Broad Street, Philadelphia, PA 19140, USA; (K.N.L.); (A.D.C.); (S.S.K.)
Xiaohua Jiang Centers for Cardiovascular Research, Inflammation, Translational and Clinical Lung Research, Metabolic Disease Research, Thrombosis Research, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA; (K.X.); (F.S.); (G.N.); (C.D.); (Y.S.); (X.J.) Centers for Metabolic Disease Research, Cardiovascular Research and Thrombosis Research, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA; (L.L.); (H.W.)
Hong Wang Centers for Metabolic Disease Research, Cardiovascular Research and Thrombosis Research, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA; (L.L.); (H.W.)
Sunil S. Karhadkar Department of Surgery, Division of Abdominal Organ Transplant, Lewis Katz School of Medicine, Temple University, 3401 N. Broad Street, Philadelphia, PA 19140, USA; (K.N.L.); (A.D.C.); (S.S.K.)
Xiaofeng Yang Centers for Cardiovascular Research, Inflammation, Translational and Clinical Lung Research, Metabolic Disease Research, Thrombosis Research, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA; (K.X.); (F.S.); (G.N.); (C.D.); (Y.S.); (X.J.) Centers for Metabolic Disease Research, Cardiovascular Research and Thrombosis Research, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA; (L.L.); (H.W.) Correspondence: (A.M.F.); (X.Y.)

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Piotrowska M, Swierczynski M, Fichna J, Piechota-Polanczyk A. The Nrf2 in the pathophysiology of the intestine: Molecular mechanisms and therapeutic implications for inflammatory bowel diseases. Pharmacol Res 2020;163:105243. [PMID: 33080322 DOI: 10.1016/j.phrs.2020.105243] [Citation(s) in RCA: 91] [Impact Index Per Article: 18.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/30/2020] [Revised: 09/29/2020] [Accepted: 10/04/2020] [Indexed: 12/14/2022]

Identification of Key Transcription Factors AP-1 and AP-1-Dependent miRNAs Forming a Co-Regulatory Network Controlling PTEN in Liver Ischemia/Reperfusion Injury. BIOMED RESEARCH INTERNATIONAL 2019;2019:8962682. [PMID: 31781649 PMCID: PMC6875376 DOI: 10.1155/2019/8962682] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 05/08/2019] [Revised: 07/07/2019] [Accepted: 07/18/2019] [Indexed: 11/18/2022]

Xiao Y, Zhang S, Li Q, Liu Z, Mai W, Chen W, Lei J, Hu H. miR-219a-5p Ameliorates Hepatic Ischemia/Reperfusion Injury via Impairing TP53BP2. Dig Dis Sci 2019;64:2177-2186. [PMID: 30796685 DOI: 10.1007/s10620-019-05535-4] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/12/2018] [Accepted: 02/14/2019] [Indexed: 12/18/2022]

Bombassaro B, Ramalho AFS, Fioravante M, Solon C, Nogueira G, Nogueira PAS, Gaspar RS, Ropelle ER, Velloso LA. CD1 is involved in diet-induced hypothalamic inflammation in obesity. Brain Behav Immun 2019;78:78-90. [PMID: 30660601 DOI: 10.1016/j.bbi.2019.01.011] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/25/2018] [Revised: 12/20/2018] [Accepted: 01/14/2019] [Indexed: 12/18/2022] Open

Wang Z, Yang W. Impaired capacity to restore proteostasis in the aged brain after ischemia: Implications for translational brain ischemia research. Neurochem Int 2018;127:87-93. [PMID: 30599146 DOI: 10.1016/j.neuint.2018.12.018] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/30/2018] [Revised: 12/28/2018] [Accepted: 12/28/2018] [Indexed: 12/15/2022]

Ischemia-Reperfusion Injury in Aged Livers-The Energy Metabolism, Inflammatory Response, and Autophagy. Transplantation 2018;102:368-377. [PMID: 29135887 DOI: 10.1097/tp.0000000000001999] [Citation(s) in RCA: 68] [Impact Index Per Article: 9.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/11/2022]

Oliva J. Proteasome and Organs Ischemia-Reperfusion Injury. Int J Mol Sci 2017;19:ijms19010106. [PMID: 29301204 PMCID: PMC5796056 DOI: 10.3390/ijms19010106] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/20/2017] [Revised: 12/12/2017] [Accepted: 12/27/2017] [Indexed: 12/17/2022] Open

Osman AS, Osman AH, Kamel MM. Study of the protective effect of ischemic and pharmacological preconditioning on hepatic ischemic reperfusion injury induced in rats. JGH OPEN 2017;1:105-111. [PMID: 30483545 PMCID: PMC6206986 DOI: 10.1002/jgh3.12018] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 08/18/2017] [Accepted: 09/29/2017] [Indexed: 12/29/2022]

Zheng X, Zhou H, Qiu Z, Gao S, Wang Z, Xiao L. Gene microarray analysis of expression profiles in liver ischemia and reperfusion. Mol Med Rep 2017;16:3299-3307. [PMID: 28713993 PMCID: PMC5548003 DOI: 10.3892/mmr.2017.6966] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/24/2016] [Accepted: 05/26/2017] [Indexed: 12/14/2022] Open

Abstract

Liver ischemia and reperfusion (I/R) injury is of primary concern in cases of liver disease worldwide and is associated with hemorrhagic shock, resection and transplantation. Numerous studies have previously been conducted to investigate the underlying mechanisms of liver I/R injury, however these have not yet been fully elucidated. To determine the difference between ischemia and reperfusion in signaling pathways and the relative pathological mechanisms, the present study downloaded microarray data GSE10657 from the Gene Expression Omnibus database. A total of two data groups from 1-year-old mice were selected for further analysis: i) A total of 90 min ischemia; ii) 90 min ischemia followed by 1 h of reperfusion, n=3 for each group. The Limma package was first used to identify the differentially expressed genes (DEGs). DEGs were subsequently uploaded to the Database for Annotation Visualization and Integrated Discovery online tool for Functional enrichment analysis. A protein-protein interaction (PPI) network was then constructed via STRING version 10.0 and analyzed using Cytoscape software. A total of 114 DEGs were identified, including 21 down and 93 upregulated genes. These DEGs were primarily enriched in malaria and influenza A, in addition to the tumor necrosis factor and mitogen activated protein kinase signaling pathways. Hub genes identified in the PPI network were C-X-C motif chemokine ligand (CXCL) 1, C-C motif chemokine ligand (CCL) 2, interleukin 6, Jun proto-oncogene, activator protein (AP)-1 transcription factor subunit, FOS proto-oncogene, AP-1 transcription factor subunit and dual specificity phosphatase 1. CXCL1 and CCL2 may exhibit important roles in liver I/R injury, with involvement in the immune and inflammatory responses and the chemokine-mediated signaling pathway, particularly at the reperfusion stage. However, further experiments to elucidate the specific roles of these mediators are required in the future.

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Lin PL, Chang JT, Wu DW, Huang CC, Lee H. Cytoplasmic localization of Nrf2 promotes colorectal cancer with more aggressive tumors via upregulation of PSMD4. Free Radic Biol Med 2016;95:121-32. [PMID: 27033953 DOI: 10.1016/j.freeradbiomed.2016.03.014] [Citation(s) in RCA: 24] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/15/2016] [Revised: 03/08/2016] [Accepted: 03/16/2016] [Indexed: 12/16/2022]

Mitochondrial Dysfunction and Autophagy in Hepatic Ischemia/Reperfusion Injury. BIOMED RESEARCH INTERNATIONAL 2015;2015:183469. [PMID: 26770970 PMCID: PMC4684839 DOI: 10.1155/2015/183469] [Citation(s) in RCA: 93] [Impact Index Per Article: 9.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 05/29/2015] [Revised: 11/10/2015] [Accepted: 11/11/2015] [Indexed: 12/26/2022]

Protein synthesis as an integral quality control mechanism during ageing. Ageing Res Rev 2015;23:75-89. [PMID: 25555680 DOI: 10.1016/j.arr.2014.12.008] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/07/2014] [Revised: 12/18/2014] [Accepted: 12/22/2014] [Indexed: 01/17/2023]

Messiha BAS, Abo-Youssef AM. Protective effects of fish oil, allopurinol, and verapamil on hepatic ischemia-reperfusion injury in rats. J Nat Sci Biol Med 2015;6:351-5. [PMID: 26283828 PMCID: PMC4518408 DOI: 10.4103/0976-9668.160003] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/01/2023] Open

Bellavista E, Martucci M, Vasuri F, Santoro A, Mishto M, Kloss A, Capizzi E, Degiovanni A, Lanzarini C, Remondini D, Dazzi A, Pellegrini S, Cescon M, Capri M, Salvioli S, D'Errico-Grigioni A, Dahlmann B, Grazi GL, Franceschi C. Lifelong maintenance of composition, function and cellular/subcellular distribution of proteasomes in human liver. Mech Ageing Dev 2014;141-142:26-34. [PMID: 25265087 DOI: 10.1016/j.mad.2014.09.003] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/12/2014] [Revised: 09/18/2014] [Accepted: 09/19/2014] [Indexed: 11/29/2022]

Affiliation(s)

Elena Bellavista Interdepartmental Centre "L. Galvani" for Integrated Studies on Biophysics, Bioinformatics and Biocomplexity (CIG), Alma Mater Studiorum, University of Bologna, 40126 Bologna, Italy; Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Alma Mater Studiorum, University of Bologna, 40126 Bologna, Italy.
Morena Martucci Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Alma Mater Studiorum, University of Bologna, 40126 Bologna, Italy.
Francesco Vasuri "F. Addarii" Institute of Oncology and Transplant Pathology at Department of Experimental, Diagnostic and Specialty Medicine (DIMES), S. Orsola-Malpighi Hospital, 40138 Bologna, Italy.
Aurelia Santoro Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Alma Mater Studiorum, University of Bologna, 40126 Bologna, Italy.
Michele Mishto Institute of Biochemistry, Charité Universitaetsmedizin Berlin, 10117 Berlin, Germany; Centro Interdipartimentale di Ricerca sul Cancro "Giorgio Prodi" (CIRC), University of Bologna, 40126 Bologna, Italy.
Alexander Kloss Institute of Biochemistry, Charité Universitaetsmedizin Berlin, 10117 Berlin, Germany.
Elisa Capizzi "F. Addarii" Institute of Oncology and Transplant Pathology at Department of Experimental, Diagnostic and Specialty Medicine (DIMES), S. Orsola-Malpighi Hospital, 40138 Bologna, Italy.
Alessio Degiovanni "F. Addarii" Institute of Oncology and Transplant Pathology at Department of Experimental, Diagnostic and Specialty Medicine (DIMES), S. Orsola-Malpighi Hospital, 40138 Bologna, Italy.
Catia Lanzarini Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Alma Mater Studiorum, University of Bologna, 40126 Bologna, Italy.
Daniel Remondini Interdepartmental Centre "L. Galvani" for Integrated Studies on Biophysics, Bioinformatics and Biocomplexity (CIG), Alma Mater Studiorum, University of Bologna, 40126 Bologna, Italy; Department of Physics and Astronomy (DIFA) and INFN Sez. Bologna, Alma Mater Studiorum, University of Bologna, 40127 Bologna, Italy.
Alessandro Dazzi Department of General Surgery and Organ Transplantation, S. Orsola-Malpighi Hospital, 40138 Bologna, Italy.
Sara Pellegrini Department of General Surgery and Organ Transplantation, S. Orsola-Malpighi Hospital, 40138 Bologna, Italy.
Matteo Cescon Department of General Surgery and Organ Transplantation, S. Orsola-Malpighi Hospital, 40138 Bologna, Italy.
Miriam Capri Interdepartmental Centre "L. Galvani" for Integrated Studies on Biophysics, Bioinformatics and Biocomplexity (CIG), Alma Mater Studiorum, University of Bologna, 40126 Bologna, Italy; Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Alma Mater Studiorum, University of Bologna, 40126 Bologna, Italy.
Stefano Salvioli Interdepartmental Centre "L. Galvani" for Integrated Studies on Biophysics, Bioinformatics and Biocomplexity (CIG), Alma Mater Studiorum, University of Bologna, 40126 Bologna, Italy; Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Alma Mater Studiorum, University of Bologna, 40126 Bologna, Italy.
Antonia D'Errico-Grigioni "F. Addarii" Institute of Oncology and Transplant Pathology at Department of Experimental, Diagnostic and Specialty Medicine (DIMES), S. Orsola-Malpighi Hospital, 40138 Bologna, Italy.
Burkhardt Dahlmann Institute of Biochemistry, Charité Universitaetsmedizin Berlin, 10117 Berlin, Germany.
Gian Luca Grazi Istituto Nazionale Tumori Regina Elena, 00144 Roma, Italy.
Claudio Franceschi Interdepartmental Centre "L. Galvani" for Integrated Studies on Biophysics, Bioinformatics and Biocomplexity (CIG), Alma Mater Studiorum, University of Bologna, 40126 Bologna, Italy; Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Alma Mater Studiorum, University of Bologna, 40126 Bologna, Italy; IRCCS Institute of Neurological Sciences, 40139 Bologna, Italy; National Research Council of Italy, CNR, Institute for Organic Synthesis and Photoreactivity (ISOF), 40129 Bologna, Italy; National Research Council of Italy, CNR, Institute of Molecular Genetics, Unit of Bologna IOR, 40136 Italy.

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Gohlke S, Mishto M, Textoris-Taube K, Keller C, Giannini C, Vasuri F, Capizzi E, D’Errico-Grigioni A, Kloetzel PM, Dahlmann B. Molecular alterations in proteasomes of rat liver during aging result in altered proteolytic activities. AGE (DORDRECHT, NETHERLANDS) 2014;36:57-72. [PMID: 23690132 PMCID: PMC3889881 DOI: 10.1007/s11357-013-9543-x] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 10/12/2012] [Accepted: 05/08/2013] [Indexed: 06/02/2023]

Kandilis AN, Karidis NP, Kouraklis G, Patsouris E, Vasileiou I, Theocharis S. Proteasome inhibitors: possible novel therapeutic strategy for ischemia–reperfusion injury? Expert Opin Investig Drugs 2013;23:67-80. [PMID: 24125540 DOI: 10.1517/13543784.2013.840287] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/14/2022]

Xu Y, Shao C, Fedorov VB, Goropashnaya AV, Barnes BM, Yan J. Molecular signatures of mammalian hibernation: comparisons with alternative phenotypes. BMC Genomics 2013;14:567. [PMID: 23957789 PMCID: PMC3751779 DOI: 10.1186/1471-2164-14-567] [Citation(s) in RCA: 40] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/21/2013] [Accepted: 08/17/2013] [Indexed: 12/12/2022] Open

Czaja MJ, Ding WX, Donohue TM, Friedman SL, Kim JS, Komatsu M, Lemasters JJ, Lemoine A, Lin JD, Ou JHJ, Perlmutter DH, Randall G, Ray RB, Tsung A, Yin XM. Functions of autophagy in normal and diseased liver. Autophagy 2013;9:1131-58. [PMID: 23774882 DOI: 10.4161/auto.25063] [Citation(s) in RCA: 363] [Impact Index Per Article: 30.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022] Open

Huang Q, Wang H, Perry SW, Figueiredo-Pereira ME. Negative regulation of 26S proteasome stability via calpain-mediated cleavage of Rpn10 subunit upon mitochondrial dysfunction in neurons. J Biol Chem 2013;288:12161-74. [PMID: 23508964 PMCID: PMC3636900 DOI: 10.1074/jbc.m113.464552] [Citation(s) in RCA: 53] [Impact Index Per Article: 4.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/25/2013] [Indexed: 12/15/2022] Open

Xia Y, Rao J, Yao A, Zhang F, Li G, Wang X, Lu L. Lithium exacerbates hepatic ischemia/reperfusion injury by inhibiting GSK-3β/NF-κB-mediated protective signaling in mice. Eur J Pharmacol 2012;697:117-25. [PMID: 23051669 DOI: 10.1016/j.ejphar.2012.09.009] [Citation(s) in RCA: 25] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/07/2012] [Revised: 09/05/2012] [Accepted: 09/17/2012] [Indexed: 11/16/2022]

Kireev RA, Cuesta S, Ibarrola C, Bela T, Moreno Gonzalez E, Vara E, Tresguerres JAF. Age-related differences in hepatic ischemia/reperfusion: gene activation, liver injury, and protective effect of melatonin. J Surg Res 2012;178:922-34. [PMID: 22647552 DOI: 10.1016/j.jss.2012.04.060] [Citation(s) in RCA: 27] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/20/2011] [Revised: 03/30/2012] [Accepted: 04/25/2012] [Indexed: 12/25/2022]

Abstract

BACKGROUND

Ischemia/reperfusion (I/R) causes functional and structural damage to liver cells, this being more pronounced with increasing age of the tissue. Melatonin is a pineal indole that has been shown to play an important role as a free radical scavenger and anti-inflammatory molecule.

MATERIAL AND METHODS

The age-dependent responses to I/R were compared in 2-mo-old and 14-mo-old male Wistar rats. After 35 min of hepatic ischemia followed by 36 h of reperfusion, rats were sacrificed. Sham-operated control rats underwent the same protocol without real vascular occlusion. Animals were intraperitoneally injected with 10 mg/kg melatonin 24 h before the operation, at the time of surgery, and 12 and 24 h after it. The tissues were submitted to histopathologic evaluation. The levels of ALT and AST were analyzed in plasma. The expression of TNF-α, IL-1β, IL-10, MCP-1, IFN-γ, iNOS, eNOS, Bad, Bax, Bcl2, AIF, PCNA, and NFKB1 genes were detected by RT-PCR in hepatic tissue.

RESULTS

I/R was associated with significant increases in the expression of pro-inflammatory and pro-apoptotic genes in liver. Older rats submitted to I/R were found to respond with increased liver damage as compared with young rats, with serum ALT and AST levels significantly higher than in young animals. Mature rats also showed more evident increases in expression of pro-inflammatory cytokines (IL-1β, MCP-1, and IFN-γ) as well as a decrease in the mRNA expression of IL-10 as compared with young animals. Pro-apoptotic genes (Bax, Bad, and AIF) were significantly enhanced in liver after I/R, without differences between young and mature animals. However, the expression of Bcl2 gene did not show any change. Melatonin treatment was able to lower the expression of pro-inflammatory cytokines and pro-apoptotic genes and to improve liver function, as indicated by normalization of plasma AST and ALT levels and by reduction of necrosis and microsteatosis areas.

CONCLUSIONS

Melatonin treatment was able to reduce the I/R-stimulated pro-inflammatory and pro-apoptotic genes in the rat liver. Since older animals showed a more marked increase in inflammation and in liver injury, the treatment was more effective in those subjects.

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Ubiquitin-proteasome system inhibitors and AMPK regulation in hepatic cold ischaemia and reperfusion injury: possible mechanisms. Clin Sci (Lond) 2012;123:93-8. [PMID: 22455352 PMCID: PMC3328266 DOI: 10.1042/cs20110093] [Citation(s) in RCA: 16] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/18/2022]

Pan LJ, Zhang ZC, Zhang ZY, Wang WJ, Xu Y, Zhang ZM. Effects and mechanisms of store-operated calcium channel blockade on hepatic ischemia-reperfusion injury in rats. World J Gastroenterol 2012;18:356-67. [PMID: 22294842 PMCID: PMC3261531 DOI: 10.3748/wjg.v18.i4.356] [Citation(s) in RCA: 9] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/03/2011] [Revised: 07/18/2011] [Accepted: 07/25/2011] [Indexed: 02/06/2023] Open

Changes of the Proteasomal System During the Aging Process. PROGRESS IN MOLECULAR BIOLOGY AND TRANSLATIONAL SCIENCE 2012;109:249-75. [DOI: 10.1016/b978-0-12-397863-9.00007-9] [Citation(s) in RCA: 51] [Impact Index Per Article: 3.9] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/21/2023]

Pan R, Liu YZ, Deng HW, Dvornyk V. Association analyses suggest the effects of RANK and RANKL on age at menarche in Chinese women. Climacteric 2011;15:75-81. [PMID: 22023082 DOI: 10.3109/13697137.2011.587556] [Citation(s) in RCA: 7] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/24/2022]

Suzuki A, Sakaguchi T, Inaba K, Suzuki S, Konno H. Impact of cell cycle disruption on impaired hepatic regeneration in aged livers with ischemic insult. J Surg Res 2010;173:267-77. [PMID: 21109256 DOI: 10.1016/j.jss.2010.10.012] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/22/2010] [Revised: 10/07/2010] [Accepted: 10/13/2010] [Indexed: 12/19/2022]

Siciliano A, Malpeli G, Platt OS, Lebouef C, Janin A, Scarpa A, Olivieri O, Amato E, Corrocher R, Beuzard Y, De Franceschi L. Abnormal modulation of cell protective systems in response to ischemic/reperfusion injury is important in the development of mouse sickle cell hepatopathy. Haematologica 2010;96:24-32. [PMID: 20851863 DOI: 10.3324/haematol.2010.028506] [Citation(s) in RCA: 25] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/11/2022] Open

Abstract

BACKGROUND

Sickle cell disease, a genetic red cell disorder inherited in an autosomal recessive manner, occurs throughout the world. Hepatic dysfunction and liver damage may be present in sickle cell disease, but the pathogenesis of these conditions is only partially understood.

DESIGN AND METHODS

Transgenic mice with sickle cell disease (SAD mice) and wild-type mice were exposed to an ischemic/reperfusion stress. The following parameters were evaluated: hematologic profile, transaminase and bilirubin levels, liver histopathology, and mRNA levels of nuclear factor-κB p65, endothelial nitric oxide synthase, inducible nitric oxide synthase, heme oxygenase-1 and phosphodiesterase-1, -2, -3, and -4 genes in hepatocytes obtained by laser-capture microdissection. Immunoblotting was used to analyze the expression of the following proteins: nuclear factor-κB p65 and phospho-nuclear factor-κB p65, heme oxygenase-1, biliverdin reductase, heat shock protein-70, heat shock protein-27 and peroxiredoxin-6. A subgroup of SAD mice was treated with the phosphodiesterase-4 inhibitor rolipram (30 mg/Kg/day by gavage) during the ischemic/reperfusion protocol.

RESULTS

In SAD mice the ischemic/reperfusion stress induced liver damage compatible with sickle cell disease hepatopathy, which was associated with: (i) lack of hypoxia-induced nuclear factor-κB p65 activation; (ii) imbalance in the endothelial/inducible nitric oxide synthase response to ischemic/reperfusion stress; (iii) lack of hypoxia-induced increased expression of heme oxygenase-1/biliverdin reductase paralleled by a compensatory increased expression of heat shock proteins 70 and 27 and peroxiredoxin-6; and (iv) up-regulation of the phosphodiesterase-1, -2, -3, and -4 genes. In SAD mice the phosphodiesterase-4 inhibitor rolipram attenuated the ischemic/reperfusion-related microcirculatory dysfunction, reduced the inflammatory cell infiltration and induced the heme oxygenase-1/biliverdin reductase cytoprotective systems.

CONCLUSIONS

In SAD mice, sickle cell hepatopathy is associated with perturbed nuclear factor-κB p65 signaling with an imbalance of endothelial/inducible nitric oxide synthase levels, lack of heme oxygenase-1/biliverdin reductase expression and up-regulation of two novel cytoprotective systems: heat shock protein-27 and peroxiredoxin-6.

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Dunston CR, Griffiths HR. The effect of ageing on macrophage Toll-like receptor-mediated responses in the fight against pathogens. Clin Exp Immunol 2010;161:407-16. [PMID: 20646005 PMCID: PMC2962957 DOI: 10.1111/j.1365-2249.2010.04213.x] [Citation(s) in RCA: 56] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 05/26/2010] [Indexed: 02/06/2023] Open

Adenosine postconditioning protects against myocardial ischemia–reperfusion injury though modulate production of TNF-α and prevents activation of transcription factor NF-kappaB. Mol Biol Rep 2010;38:531-8. [DOI: 10.1007/s11033-010-0137-8] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/20/2009] [Accepted: 03/23/2010] [Indexed: 12/18/2022]