beta-arrestin 1 mediates liver thyrotropin regulation of cholesterol conversion metabolism via the akt-dependent pathway

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2018
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Abstract
After activation, G protein-coupled receptors (GPCRs) are desensitized by β-arrestins (ARRBs). Moreover, ARRBs can initiate a second wave of signaling independent of G proteins. Thyroid-stimulating hormone receptor (TSHR) is one of the GPCR members. In our previous study, TSHR was identified in the liver; the major role of TSHR in cholesterol metabolism was illustrated, as TSH could regulate hepatic cholesterol metabolism via cAMP/PKA/CREB/HMGCR and SREBP2/HNF4α/CYP7A1 pathways. It has been reported that ARRB2 predominates over ARRB1 in TSHR internalization. However, the significance of ARRBs in TSH-initiated cholesterol metabolism has not been illustrated. In our study, the effects of ARRBs on TSH-regulated cholesterol metabolism are investigated. ARRB1/2 was genetically inactivated in C57BL/6 mice and HepG2 cell line, respectively. Cholesterol levels in arrestin-knockout mice and arrestin-knockdown cells were measured. Molecules participating in cholesterol metabolism were analyzed. It turned out that deficiencies in ARRB1 led to decreased cholesterol levels and decreased TSH-stimulated AKT phosphorylation. Subsequently, the inhibitory effect on CYP7A1 by SREBP2 was reduced due to lowered mature SREBP2 level. Other than the failures of TSH in ARRB-knockdown cells, the AKT activator SC79 could enhance AKT phosphorylation and mature SREBP2 level. Our results demonstrate that ARRBs, especially ARRB1, are involved in TSH-regulated cholesterol metabolism through the AKT pathway.
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niu2018internationalbeta-arrestin Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Shaona Niu;Hui Li;Wenbin Chen;Jiajun Zhao;Ling Gao;Tao Bo
Journal zhonghua wei zhong bing ji jiu yi xue
Year 2018
DOI
10.1155/2018/4371396
URL
http://dx.doi.org/10.1155/2018/4371396
Keywords
clinical endocrinology diseases of the endocrine glands

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