Published online May 27, 2020. doi: 10.4240/wjgs.v12.i5.226
Peer-review started: December 18, 2019
First decision: January 6, 2020
Revised: March 13, 2020
Accepted: April 18, 2020
Article in press: April 18, 2020
Published online: May 27, 2020
Processing time: 161 Days and 4.5 Hours
Loss and/or dysfunction of interstitial Cajal-like cells (ICLCs) in the gallbladder may promote cholesterol gallstone formation by decreasing gallbladder motility.
To study the effect of cholesterol on the proliferation and apoptosis of ICLCs from guinea pig gallbladders.
Guinea pig gallbladder ICLCs were isolated and cultured in vitro. The cells were exposed to cholesterol solutions at different concentrations (0, 25, 50, and 100 mg/L) for 24 h. Then, cell proliferation was detected by the CCK-8 method and the apoptosis rate was detected by flow cytometry. Further, the expression of the c-Kit protein was detected by Western blot and the expression level of c-Kit mRNA in the cells was detected by real-time quantitative PCR.
After ICLCs were cultured with cholesterol at concentrations of 25, 50, and 100 mg/L, the proliferation rates decreased significantly (P < 0.05), whereas the apoptosis rates increased significantly (P < 0.05). Moreover, the expression of c-Kit protein and mRNA decreased significantly (P < 0.05).
High cholesterol concentrations can inhibit the proliferation of ICLCs and promote apoptosis. This decrease in the ICLC proliferation rate might be caused by the inhibition of the stem cell factor/c-Kit signaling pathway.
Core tip: Interstitial Cajal-like cells (ICLCs) in the gallbladder have been reported to play an important role in the regulation of gallbladder motility. Loss and/or dysfunction of ICLCs may contribute to motion abnormality of the gallbladder and promote cholesterol gallstone formation. Absorption of supersaturated cholesterol in bile by the gallbladder wall might be the cause of reductions in gallbladder ICLCs. This study evaluated the effect of cholesterol on the proliferation and apoptosis of ICLCs from guinea pig gallbladders. We found that high concentrations of cholesterol can inhibit the proliferation of ICLCs and promote apoptosis. This decrease in the ICLC proliferation rate might be caused by the inhibition of the stem cell factor/c-Kit signaling pathway. ICLCs may serve as an alternative treatment target for preventing cholesterol gallstones.