PMID- 27384152
OWN - NLM
STAT- MEDLINE
DCOM- 20180529
LR  - 20211025
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 6
DP  - 2016 Jul 7
TI  - miR-7a/b attenuates post-myocardial infarction remodeling and protects H9c2 
      cardiomyoblast against hypoxia-induced apoptosis involving Sp1 and PARP-1.
PG  - 29082
LID - 10.1038/srep29082 [doi]
LID - 29082
AB  - miRs (microRNAs, miRNAs) intricately regulate physiological and pathological 
      processes. Although miR-7a/b protects against cardiomyocyte injury in 
      ischemia/reperfusion injury, the function of miR-7a/b in myocardial infarction 
      (MI)-induced cardiac remodeling remains unclear. Here, we sought to investigate 
      the function of miR-7a/b in post-MI remodeling in a mouse model and to determine 
      the underlying mechanisms involved. miR-7a/b overexpression improved cardiac 
      function, attenuated cardiac remodeling and reduced fibrosis and apoptosis, 
      whereas miR-7a/b silencing caused the opposite effects. Furthermore, miR-7a/b 
      overexpression suppressed specific protein 1 (Sp1) and poly (ADP-ribose) 
      polymerase (PARP-1) expression both in vivo and in vitro, and a luciferase 
      reporter activity assay showed that miR-7a/b could directly bind to Sp1. 
      Mithramycin, an inhibitor of the DNA binding activity of Sp1, effectively 
      repressed PARP-1 and caspase-3, whereas knocking down miR-7a/b partially 
      counteracted these beneficial effects. Additionally, an immunoprecipitation assay 
      indicated that hypoxia triggered activation of the binding activity of Sp1 to the 
      promoters of PARP-1 and caspase-3, which is abrogated by miR-7a/b. In summary, 
      these findings identified miR-7a/b as protectors of cardiac remodeling and 
      hypoxia-induced injury in H9c2 cardiomyoblasts involving Sp1 and PARP-1.
FAU - Li, Rui
AU  - Li R
AD  - Department of Health Care, China-Japan Friendship Hospital, Ministry of Health, 
      Beijing, China.
FAU - Geng, Hai-Hua
AU  - Geng HH
AD  - The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese 
      Ministry of Education and Chinese Ministry of Public Health, Qilu Hospital of 
      Shandong University, Jinan, Shandong, China.
FAU - Xiao, Jie
AU  - Xiao J
AD  - The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese 
      Ministry of Education and Chinese Ministry of Public Health, Qilu Hospital of 
      Shandong University, Jinan, Shandong, China.
FAU - Qin, Xiao-Teng
AU  - Qin XT
AD  - The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese 
      Ministry of Education and Chinese Ministry of Public Health, Qilu Hospital of 
      Shandong University, Jinan, Shandong, China.
FAU - Wang, Fu
AU  - Wang F
AD  - The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese 
      Ministry of Education and Chinese Ministry of Public Health, Qilu Hospital of 
      Shandong University, Jinan, Shandong, China.
FAU - Xing, Jun-Hui
AU  - Xing JH
AD  - The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese 
      Ministry of Education and Chinese Ministry of Public Health, Qilu Hospital of 
      Shandong University, Jinan, Shandong, China.
FAU - Xia, Yan-Fei
AU  - Xia YF
AD  - The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese 
      Ministry of Education and Chinese Ministry of Public Health, Qilu Hospital of 
      Shandong University, Jinan, Shandong, China.
FAU - Mao, Yang
AU  - Mao Y
AD  - The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese 
      Ministry of Education and Chinese Ministry of Public Health, Qilu Hospital of 
      Shandong University, Jinan, Shandong, China.
FAU - Liang, Jing-Wen
AU  - Liang JW
AD  - The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese 
      Ministry of Education and Chinese Ministry of Public Health, Qilu Hospital of 
      Shandong University, Jinan, Shandong, China.
FAU - Ji, Xiao-Ping
AU  - Ji XP
AD  - The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese 
      Ministry of Education and Chinese Ministry of Public Health, Qilu Hospital of 
      Shandong University, Jinan, Shandong, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160707
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (MIRN7 microRNA, mouse)
RN  - 0 (MicroRNAs)
RN  - 0 (Sp1 Transcription Factor)
RN  - EC 2.4.2.30 (Poly (ADP-Ribose) Polymerase-1)
RN  - EC 3.4.22.- (Caspase 3)
RN  - NIJ123W41V (Plicamycin)
SB  - IM
MH  - Animals
MH  - Apoptosis/genetics
MH  - Atrial Remodeling/genetics
MH  - Caspase 3/genetics
MH  - Cell Hypoxia/genetics
MH  - DNA-Binding Proteins/genetics
MH  - Disease Models, Animal
MH  - Gene Expression Regulation/drug effects
MH  - Humans
MH  - Mice
MH  - MicroRNAs/*genetics
MH  - Myocardial Infarction/*genetics/physiopathology
MH  - Myocytes, Cardiac/metabolism/pathology
MH  - Plicamycin/administration & dosage
MH  - Poly (ADP-Ribose) Polymerase-1/*genetics
MH  - Reperfusion Injury/*genetics/pathology
MH  - Sp1 Transcription Factor/*genetics
PMC - PMC4935883
EDAT- 2016/07/08 06:00
MHDA- 2018/05/31 06:00
PMCR- 2016/07/07
CRDT- 2016/07/08 06:00
PHST- 2016/01/28 00:00 [received]
PHST- 2016/06/09 00:00 [accepted]
PHST- 2016/07/08 06:00 [entrez]
PHST- 2016/07/08 06:00 [pubmed]
PHST- 2018/05/31 06:00 [medline]
PHST- 2016/07/07 00:00 [pmc-release]
AID - srep29082 [pii]
AID - 10.1038/srep29082 [doi]
PST - epublish
SO  - Sci Rep. 2016 Jul 7;6:29082. doi: 10.1038/srep29082.