PMID- 36300016
OWN - NLM
STAT- MEDLINE
DCOM- 20221028
LR  - 20221028
IS  - 2314-7156 (Electronic)
IS  - 2314-8861 (Print)
IS  - 2314-7156 (Linking)
VI  - 2022
DP  - 2022
TI  - Adiponectin Protects Hypoxia/Reoxygenation-Induced Cardiomyocyte Injury by 
      Suppressing Autophagy.
PG  - 8433464
LID - 10.1155/2022/8433464 [doi]
LID - 8433464
AB  - Adiponectin is a cytokine produced by adipocytes and acts as a potential 
      cardioprotective agent and plays an important role in myocardial 
      ischemia/reperfusion injury. In a myocardial hypoxia/reoxygenation model using 
      neonatal rat ventricular myocytes, we investigated the contribution of 
      adiponectin-mediated autophagy to its cardioprotective effects. Cardiomyocytes 
      were exposed to hypoxia/reoxygenation pretreated with or without adiponectin in 
      the presence of absence of rapamycin. Cell viability was analyzed using the 
      3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method. Western 
      blotting assay was used to determine the expression levels of 
      microtubule-associated proteins 1A/1B light chain 3B (LC3B), adenosine 
      monophosphate-activated protein kinase (AMPK), mammalian target of rapamycin 
      (mTOR), p62/sequestosome 1, unc-51 like autophagy activating kinase 1 (ULK1), and 
      Beclin-1. Autophagosome formation was detected by monodansylcadaverine staining. 
      We found that hypoxia induced a time dependent decline in cardiomyocyte 
      viability, and increase in autophagy and reoxygenation further augmented 
      hypoxia-induced autophagy induction and consequently reduced cell viability. 
      Adiponectin treatment alleviated hypoxia/reoxygenation-induced cellular damage 
      and autophagy in cardiomyocytes. Adiponectin treatment also attenuated 
      hypoxia/reoxygenation-promoted cardiomyocyte autophagy even in the presence of 
      another autophagy stimulator rapamycin in part by inhibiting vacuolar 
      hydron-adenosine triphosphatase. Additionally, autophagy suppression by 
      adiponectin during hypoxia/reoxygenation was associated with the attenuated 
      phosphorylation of AMPK and ULK1, augmented phosphorylation of mTOR, and the 
      reduced protein expression levels of Beclin-1 in cardiomyocytes. Taken together, 
      these results suggest that adiponectin protects ischemia/reperfusion-induced 
      cardiomyocytes by suppressing autophagy in part through AMPK/mTOR/ULK1/Beclin-1 
      signaling pathway.
CI  - Copyright (c) 2022 Jia Guo et al.
FAU - Guo, Jia
AU  - Guo J
AUID- ORCID: 0000-0002-4574-4543
AD  - Center for Hypertension Care, Shanxi Medical University First Hospital, Taiyuan, 
      Shanxi, China.
FAU - Zhu, Kaiyi
AU  - Zhu K
AUID- ORCID: 0000-0002-0727-6996
AD  - Center for Hypertension Care, Shanxi Medical University First Hospital, Taiyuan, 
      Shanxi, China.
FAU - Li, Zhidong
AU  - Li Z
AD  - Department of Pharmacology, Shanxi Medical University, Taiyuan, Shanxi, China.
FAU - Xiao, Chuanshi
AU  - Xiao C
AD  - Center for Hypertension Care, Shanxi Medical University First Hospital, Taiyuan, 
      Shanxi, China.
LA  - eng
PT  - Journal Article
DEP - 20221017
PL  - Egypt
TA  - J Immunol Res
JT  - Journal of immunology research
JID - 101627166
RN  - 0 (Beclin-1)
RN  - 0 (Adiponectin)
RN  - EC 2.7.11.1 (Autophagy-Related Protein-1 Homolog)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
RN  - 0 (Cardiotonic Agents)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - 0 (Microtubule-Associated Proteins)
RN  - W36ZG6FT64 (Sirolimus)
RN  - 0 (Cytokines)
RN  - 415SHH325A (Adenosine Monophosphate)
RN  - EC 3.6.1.- (Adenosine Triphosphatases)
SB  - IM
MH  - Rats
MH  - Animals
MH  - *Myocytes, Cardiac/metabolism
MH  - Beclin-1/metabolism/pharmacology
MH  - *Adiponectin
MH  - Autophagy-Related Protein-1 Homolog/metabolism
MH  - AMP-Activated Protein Kinases/metabolism
MH  - Cardiotonic Agents/metabolism/pharmacology
MH  - Apoptosis
MH  - Autophagy
MH  - TOR Serine-Threonine Kinases/metabolism
MH  - Hypoxia/metabolism
MH  - Microtubule-Associated Proteins/metabolism/pharmacology
MH  - Sirolimus/pharmacology
MH  - Cytokines/metabolism
MH  - Adenosine Monophosphate/metabolism/pharmacology
MH  - Adenosine Triphosphatases/metabolism/pharmacology
MH  - Mammals/metabolism
PMC - PMC9592213
COIS- The authors declare no conflicts of interest.
EDAT- 2022/10/28 06:00
MHDA- 2022/10/29 06:00
PMCR- 2022/10/17
CRDT- 2022/10/27 02:39
PHST- 2022/08/20 00:00 [received]
PHST- 2022/10/08 00:00 [accepted]
PHST- 2022/10/27 02:39 [entrez]
PHST- 2022/10/28 06:00 [pubmed]
PHST- 2022/10/29 06:00 [medline]
PHST- 2022/10/17 00:00 [pmc-release]
AID - 10.1155/2022/8433464 [doi]
PST - epublish
SO  - J Immunol Res. 2022 Oct 17;2022:8433464. doi: 10.1155/2022/8433464. eCollection 
      2022.