Published online Mar 26, 2023. doi: 10.4252/wjsc.v15.i3.90
Peer-review started: June 30, 2022
First decision: December 30, 2022
Revised: January 6, 2023
Accepted: February 16, 2023
Article in press: February 16, 2023
Published online: March 26, 2023
Processing time: 265 Days and 18.4 Hours
Anoikis plays a limiting role in the therapeutic efficacy of mesenchymal stem cells (MSCs). As a proapoptotic molecule, mammalian Ste20-like kinase 1 (Mst1) can increase the production of reactive oxygen species (ROS), thereby promoting anoikis. Recently, Mst1 inhibition was found to protect mouse bone marrow MSCs (mBMSCs) from H2O2-induced cell apoptosis by inducing autophagy and reducing ROS production. However, the influence of Mst1 inhibition on anoikis in mBMSCs remains unclear.
To investigate whether Mst1 inhibition could reduce anoikis in isolated mBMSCs.
To investigate the mechanisms by which Mst1 inhibition acts on anoikis in isolated mBMSCs.
Poly-2-hydroxyethyl methacrylate-induced anoikis was used following Mst1 inhibition in mBMSCs. Integrin (ITGs) levels were tested by flow cytometry. Autophagy and ITGα5β1 were inhibited using 3-methyladenine and small interfering RNA, respectively. The alterations in anoikis were evaluated by Terminal-deoxynucleoitidyl Transferase Mediated Nick End Labeling and anoikis assays. The levels of the anoikis-related proteins ITGα5, ITGβ1, and phospho-focal adhesion kinase, which activate caspase 3, and the autophagy-related proteins microtubules associated protein 1 light chain 3 II/I, Beclin1 and p62 were detected by Western blotting.
In isolated mBMSCs, Mst1 expression was upregulated, and Mst1 inhibition significantly reduced cell apoptosis, induced autophagy and decreased ROS levels. Mechanistically, we found that Mst1 inhibition upregulated ITGα5 and ITGβ1 expression but not ITGα4, ITGαv, or ITGβ3 expression. Moreover, ITGα5β1 upregulation and autophagy induction by Mst1 inhibition played an essential role in terms of the protective efficacy of Mst1 inhibition on averting anoikis.
Mst1 inhibition ameliorated autophagy formation, increased ITGα5β1 expression, and decreased the excessive production of ROS, thereby reducing cell apoptosis in isolated mBMSCs. On this basis, Mst1 inhibition may provide a promising strategy to overcome the anoikis of transplanted MSCs.
In isolated mBMSCs, Mst1 inhibition ameliorated not only autophagy formation but also ITGα5β1 expression (not ITGα4, ITGαv, or ITGβ3). Mst1 inhibition-induced autophagy scavenged excessive ITGα5β1-triggered ROS. Consequently, Mst1 inhibition-based infusion may improve the therapeutic efficacy of MSCs, thereby serving as an ideal candidate for clinical transplantation in pulmonary arterial hypertension.