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Altered absorptive function in the gall bladder during cholesterol gallstone formation is associated with abnormal
Yongsheng Chen1, Shuodong Wu2, Li Qi3
1Department of General Surgery, Shengjing Hospital of China Medical University, No. 36, San Hao Street, Heping District, Shenyang, 110004, Liaoning Province, China.
Journal of Physiology and Biochemistry
|June 20, 2020
Summary
Dysfunction of the sodium-hydrogen exchanger 3 (NHE3) is linked to cholesterol gallstones. Abnormal NHE3 complex formation, involving ezrin and NHERF1, is associated with gallstone development, potentially initiated by decreased bile taurochenodeoxycholate (TCDC).
Area of Science:
- Cellular and Molecular Biology
- Gastroenterology
- Biochemistry
Background:
- Cholesterol gallstone formation is a significant health issue.
- The sodium-hydrogen exchanger 3 (NHE3) plays a role in gallbladder function.
- NHE3 dysfunction has been implicated in the pathogenesis of gallstones.
Purpose of the Study:
- To investigate the association between NHE3 dysfunction and abnormalities in NHE3 complex formation.
- To explore the role of ezrin and NHERF1 in NHE3 complex formation during gallstone development.
- To identify potential initiating factors for NHE3 dysfunction in the context of gallstones.
Main Methods:
- Mice were fed control or lithogenic diets to induce gallstones.
- Expression of NHE3, ezrin, and NHERF1 was analyzed using RT-PCR and western blot.
- Immunofluorescence and immunoprecipitation were used to study protein interactions and localization.
- Cholangiocarcinoma cells were stimulated with taurochenodeoxycholate (TCDC) and forskolin to mimic cellular conditions.
Main Results:
- NHERF1 expression and ezrin phosphorylation increased in gallbladder epithelial cells of mice with gallstones.
- Ezrin formed macrocomplexes with NHE3, with enhanced interaction observed after gallstone formation.
- TCDC, in conjunction with forskolin, stimulated ezrin phosphorylation and enhanced NHE3-ezrin interaction in cholangiocarcinoma cells.
- TCDC increased cAMP accumulation and NHERF1/PKCα expression.
Conclusions:
- Cholesterol gallstone formation is associated with abnormal NHE3 complex formation.
- Altered interactions between NHE3, ezrin, and NHERF1 contribute to gallstone pathogenesis.
- Decreased biliary TCDC may be an initiating factor leading to abnormal gallbladder absorption and gallstone formation.
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