PMID- 31401190
OWN - NLM
STAT- MEDLINE
DCOM- 20200225
LR  - 20211204
IS  - 1638-6183 (Electronic)
IS  - 0300-9084 (Linking)
VI  - 165
DP  - 2019 Oct
TI  - Apolipoprotein A-I improves hepatic autophagy through the AMPK pathway.
PG  - 210-218
LID - S0300-9084(19)30233-0 [pii]
LID - 10.1016/j.biochi.2019.08.001 [doi]
AB  - Dysfunction in lipid metabolism may result in a decrease in hepatic autophagy, 
      which contributes to the pathogenesis of non-alcoholic steatohepatitis. 
      ATP-binding cassette transporter A1 transports free cholesterol and phospholipids 
      to apolipoprotein A-I (apoA-I) to form nascent high-density lipoprotein 
      particles. Results from previous studies showed that the overexpression of apoA-I 
      significantly reduced levels of hepatic lipids and endoplasmic reticulum stress 
      by modifying lipid transport. Here, we investigated the effects of apoA-I 
      overexpression on hepatic autophagy in cultured hepatocytes and mice. The 
      overexpression of apoA-I in HepG2 cells resulted in an increase in the levels of 
      autophagy as well as the phosphorylation of AMP-activated protein kinase alpha 
      (AMPKalpha) and ULK1 and a decrease in the phosphorylation of mammalian target of 
      rapamycin (mTOR). An AMPK inhibitor and siRNA eliminated this apoA-I effect. 
      Consistently, apoA-I transgenic mice showed increased autophagy and AMPKalpha 
      phosphorylation. These results suggest that apoA-I overexpression alleviates 
      steatohepatitis by increasing hepatic autophagy through the AMPK-mTOR-ULK1 
      pathway.
CI  - Copyright (c) 2019 Elsevier B.V. and Societe Francaise de Biochimie et Biologie 
      Moleculaire (SFBBM). All rights reserved.
FAU - Rao, Xia
AU  - Rao X
AD  - Department of Cell Biology, Municipal Laboratory for Liver Protection and 
      Regulation of Regeneration, School of Basic Medical Sciences, Capital Medical 
      University, Beijing, 100069, China.
FAU - Wang, Yutong
AU  - Wang Y
AD  - Department of Cell Biology, Municipal Laboratory for Liver Protection and 
      Regulation of Regeneration, School of Basic Medical Sciences, Capital Medical 
      University, Beijing, 100069, China. Electronic address: yutongw@ccmu.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20190808
PL  - France
TA  - Biochimie
JT  - Biochimie
JID - 1264604
RN  - 0 (APOA1 protein, human)
RN  - 0 (Apolipoprotein A-I)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (Autophagy-Related Protein-1 Homolog)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.1 (ULK1 protein, human)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
SB  - IM
MH  - AMP-Activated Protein Kinases/antagonists & inhibitors/*metabolism
MH  - Animals
MH  - Apolipoprotein A-I/*physiology
MH  - Autophagy
MH  - Autophagy-Related Protein-1 Homolog/*metabolism
MH  - Fatty Liver/*metabolism
MH  - Hep G2 Cells
MH  - Hepatocytes/cytology/*metabolism
MH  - Humans
MH  - Intracellular Signaling Peptides and Proteins/*metabolism
MH  - Lipid Metabolism
MH  - Liver/cytology/*metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - TOR Serine-Threonine Kinases/*metabolism
OTO - NOTNLM
OT  - AMP-Activated protein kinase
OT  - Apolipoprotein A-I
OT  - Autophagy
OT  - Steatohepatitis
EDAT- 2019/08/12 06:00
MHDA- 2020/02/26 06:00
CRDT- 2019/08/12 06:00
PHST- 2019/03/11 00:00 [received]
PHST- 2019/08/05 00:00 [accepted]
PHST- 2019/08/12 06:00 [pubmed]
PHST- 2020/02/26 06:00 [medline]
PHST- 2019/08/12 06:00 [entrez]
AID - S0300-9084(19)30233-0 [pii]
AID - 10.1016/j.biochi.2019.08.001 [doi]
PST - ppublish
SO  - Biochimie. 2019 Oct;165:210-218. doi: 10.1016/j.biochi.2019.08.001. Epub 2019 Aug 
      8.