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.
Absorption of supersaturated cholesterol in bile by the gallbladder wall might be the cause of loss and/or dysfunction of gallbladder ICLCs.
The present study aimed to evaluate the effect of cholesterol on the proliferation and apoptosis of ICLCs from guinea pig gallbladders.
ICLCs from guinea pig gallbladders were isolated and cultured in vitro. The cells were exposed to cholesterol solutions at different concentrations. Cell proliferation, apoptosis rate, and expression of c-Kit protein and mRNA were detected.
Compared with the control group (no treatment group), the addition of cholesterol significantly decreased the proliferation rates and the expression of c-Kit protein and mRNA in ICLCs. While, the apoptosis rates of cells were increased.
High cholesterol concentrations can inhibit the proliferation of ICLCs and promote apoptosis, which might be caused by the inhibition of the stem cell factor/c-Kit signaling pathway.
This is a proof-of-concept study that lacks a mechanical study. The mechanism by which cholesterol regulates the stem cell factor/c-Kit pathway remains unclear and need further investigation.