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Effect of cholesterol on in vitro cultured interstitial Cajal-like cells isolated from guinea pig gallbladders

BACKGROUND: Loss and/or dysfunction of interstitial Cajal-like cells (ICLCs) in the gallbladder may promote cholesterol gallstone formation by decreasing gallbladder motility. AIM: To study the effect of cholesterol on the proliferation and apoptosis of ICLCs from guinea pig gallbladders. METHODS: G...

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Detalles Bibliográficos
Autores principales: Fu, Bei-Bei, Xu, Jin-Huang, Wu, Shuo-Dong, Fan, Ying
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Baishideng Publishing Group Inc 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7289650/
https://www.ncbi.nlm.nih.gov/pubmed/32551028
http://dx.doi.org/10.4240/wjgs.v12.i5.226
Descripción
Sumario:BACKGROUND: Loss and/or dysfunction of interstitial Cajal-like cells (ICLCs) in the gallbladder may promote cholesterol gallstone formation by decreasing gallbladder motility. AIM: To study the effect of cholesterol on the proliferation and apoptosis of ICLCs from guinea pig gallbladders. METHODS: 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. RESULTS: 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). CONCLUSION: 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.