HCBP6 maintaining of cholesterol homeostasis by down-regulating SREBP2/HMGCR

International Meeting on Clinical Case Reports

April 18-20, 2016 Dubai, UAE

Jun Cheng, Zhang Y, Gao L L, Liu S A, Han M, Liang P, Lu H P and Feng S H

Capital Medical University, China

Posters & Accepted Abstracts: J Clin Case Rep

Abstract :

Dysregulation of cholesterol homeostasis is associated with metabolic diseases including fatty liver, atherosclerosis and type-2 diabetes. Growing evidences have suggested that the nucleocapsid of HCV (core) involves in lipid droplet accumulation, changes lipogenic gene expression and/or its activity. However, as a HCV core protein interacting protein, the function of HCBP6 protein is remains unclear. Here, we found that overexpression of HCBP6 in hepatoma cells suppressed the expression of sterol response element binding protein2 (SREBP2) that is a crucial factor for maintaining cholesterol homeostasis and HMGCR expression. Consistently, we found that silence of HCBP6 expression in hepatoma cells induced SREBP2 expression and eventually increased intracellular cholesterol biosynthesis. Moreover, HCBP6 expression level was reduced in liver tissue of mice fed with a high-fat diet and this decrease correlated with an increase of total cholesterol level. Thus, HCBP6 controls cholesterol homeostasis through regulating SREBP2 and HMGCR expressions and their activities. We also found that miR-185 regulated HCBP6 expression through a complex cholesterol-responsive feedback loop. In conclusion, we provide evidence that a mir-185 mediated HCBP6 expression maintaining of cholesterol homeostasis by down-regulating SREBP2/HMGCR.

Biography :

Email: chengj0817@sina.cn