PMID- 30450663
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230201
IS  - 1097-4644 (Electronic)
IS  - 0730-2312 (Linking)
VI  - 120
IP  - 5
DP  - 2019 May
TI  - Activation of the mammalian target of rapamycin signaling pathway underlies a 
      novel inhibitory role of ring finger protein 182 in ventricular remodeling after 
      myocardial ischemia-reperfusion injury.
PG  - 7635-7648
LID - 10.1002/jcb.28038 [doi]
AB  - Myocardial ischemia-reperfusion injury (MIRI) is a major cause of cardiovascular 
      disease, leading to mortality and disability associated with coronary occlusion 
      worldwide. A correlation of mammalian target of rapamycin (mTOR)/nuclear 
      factor-kappa B (NF-kappaB) signaling pathway has been observed with brain damage 
      resulting from myocardial ischemia. Therefore, by establishing MIRI rat model, 
      this study aimed to explore whether ring finger protein 182 (RNF182) regulates 
      the mTOR signaling pathway affecting MIRI. Initially, MIRI rat model was 
      successfully established, followed by either treatment of shRNF182 or 
      phosphoesterase (PITE) (inhibitor of the mTOR signaling pathway). Then, the serum 
      levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and 
      malondialdehyde (MDA), left ventricular ejection fraction (LVEF), left 
      ventricular fractional shortening (LVFS), left ventricular systolic pressure 
      (LVSP), and left ventricular end-diastolic pressure (LVEDP) were determined, 
      followed by detection of myocardial infarct sizes and myocardial cell apoptosis. 
      Moreover, the levels of related genes/proteins were determined to further 
      determine the mechanisms of RNF182 in MIRI. First, RNF182 was upregulated in 
      MIRI. Another key observation of this study was that rats with shRNF182 presented 
      with downregulated SOD, GSH-Px, and MDA in serum, accompanied by decreased levels 
      of LVEF, LVFS, LVSP, and LVEDP. In addition, both reduced myocardial infarct 
      sizes and apoptosis of myocardial cells were observed after silencing RNF182. 
      Furthermore, silencing of the RNF182 was observed to downregulate Bcl 
      2-associated X and cysteine proteinase 3 but upregulate mTOR, ribosome protein 
      subunit 6 kinase 1, eukaryotic elongation factor 2, and B-cell lymphoma-2. 
      Importantly, the effects of RNF182 silencing were reversed after PITE treatment. 
      In conclusion, our study demonstrates that RNF182 silencing can prevent 
      ventricular remodeling in rats after MIRI by activating the mTOR signaling 
      pathway.
CI  - (c) 2018 Wiley Periodicals, Inc.
FAU - Wang, Jing-Hua
AU  - Wang JH
AD  - Department of Pediatric Rheumatology, Immunology and Allergy, The First Hospital 
      of Jilin University, Changchun, China.
FAU - Wei, Zhi-Feng
AU  - Wei ZF
AD  - Department of Cardiology, FAW General Hospital, Changchun, China.
FAU - Gao, Yan-Li
AU  - Gao YL
AD  - Department of Science and Education, The First Hospital of Jilin University, 
      Changchun, China.
FAU - Liu, Cong-Cong
AU  - Liu CC
AD  - Department of Pediatric Rheumatology, Immunology and Allergy, The First Hospital 
      of Jilin University, Changchun, China.
FAU - Sun, Jing-Hui
AU  - Sun JH
AUID- ORCID: 0000-0001-6040-489X
AD  - Department of Pediatric Cardiology, The First Hospital of Jilin University, 
      Changchun, China.
LA  - eng
PT  - Journal Article
DEP - 20181118
PL  - United States
TA  - J Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
SB  - IM
OTO - NOTNLM
OT  - gene silencing
OT  - mammalian target of rapamycin (mTOR) signaling pathway
OT  - myocardial ischemia-reperfusion injury (MIRI)
OT  - ring finger protein 182 (RNF182)
OT  - ventricular remodeling
EDAT- 2018/11/20 06:00
MHDA- 2018/11/20 06:01
CRDT- 2018/11/20 06:00
PHST- 2018/07/09 00:00 [received]
PHST- 2018/10/15 00:00 [accepted]
PHST- 2018/11/20 06:00 [pubmed]
PHST- 2018/11/20 06:01 [medline]
PHST- 2018/11/20 06:00 [entrez]
AID - 10.1002/jcb.28038 [doi]
PST - ppublish
SO  - J Cell Biochem. 2019 May;120(5):7635-7648. doi: 10.1002/jcb.28038. Epub 2018 Nov 
      18.