The miR-378/PGC1β/mTOR axis as an alternative mechanism to promote autophagy during adipogenesis

Lyu, Qing; Huang, Nunu; Dong, Kunzhe; Xie, Weidong; He, Jie; Xu, Ning; Zhang, Yaou

doi:10.1016/j.bbalip.2021.158921

Cited by 1 publication

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“…The biological function of miRNA in hepatic lipid metabolism is an inspiration to expound the molecular mechanism of CADE improving alcohol-caused lipidosis from the perspective of gene regulation. A recent study indicated that miR-378b, which showed great activities to be involved in lipid regulation and systemic energy homeostasis [ 22–24 ], is elevated by ethanol in C57BL/6 mice [ 25 ]. Additionally, another research reported that miR-378b negatively regulated CaMKK2, which was served as a key regulator to balance energy both in cells and the whole organism, participating in lipid metabolism [ 26 ].…”

Section: Introductionmentioning

confidence: 99%

Caffeic acid dimethyl ether alleviates alcohol-induced hepatic steatosis via microRNA-378b-mediated CaMKK2-AMPK pathway

Zhang

Wang

et al. 2022

Bioengineered

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Alcoholic liver disease (ALD), with its increasing morbidity and mortality, has seriously and extensively affected the health of people worldwide. Caffeic Acid Dimethyl Ether (CADE) significantly inhibits alcohol-induced hepatic steatosis in vivo through AMP-activated protein kinase (AMPK) pathway, but its in-depth mechanism remains unclear. This work aimed to clarify further mechanism of CADE in improving hepatic lipid accumulation in ALD through the microRNA-378b (miR-378b)-mediated Ca2+/calmodulin-dependent protein kinase kinase 2 (CaMKK2)-AMPK signaling pathway. Here, we reported that the hepatic or serum triglyceride (TG), total cholesterol (TC), alanine aminotransferase (ALT), and aspartate transaminase (AST) levels were sharply escalated by ethanol while prominently decreased by CADE. Ethanol sharply up-regulated miR-378b expression while CADE effectively prevented the elevation of miR-378b in vivo . And treatment of CADE surely increased mRNA and protein expression of CaMKK2 as a kinase of AMPK and reduced lipid accumulation in the livers of alcohol-fed C57BL/6 mice. MiR-378b escalation exacerbated hepatic steatosis and inhibited CaMKK2-AMPK signaling, while miR-378b deficiency alleviated lipid accumulation and activated the CaMKK2 cascade. Furthermore, CADE alleviated the lipid deposition and reversed the disorder of CaMKK2-AMPK signaling pathway induced by miR-378b over-expression. However, knockdown of miR-378b eliminated the beneficial effect of CADE on lipid metabolism. In brief, our results showed that CADE ultimately improved hepatic lipid deposition by regulating the CaMKK2-AMPK signaling pathway through miR-378b.

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Section: Introductionmentioning

confidence: 99%