PMID- 27121079
OWN - NLM
STAT- MEDLINE
DCOM- 20170216
LR  - 20231213
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Linking)
VI  - 13
IP  - 6
DP  - 2016 Jun
TI  - MicroRNA‑451 protects against cardiomyocyte anoxia/reoxygenation injury by 
      inhibiting high mobility group box 1 expression.
PG  - 5335-41
LID - 10.3892/mmr.2016.5192 [doi]
AB  - High mobility group box 1 (HMGB1) protein serves an important role in myocardial 
      ischemia/reperfusion (I/R) injury. MicroRNAs (miRNAs) are a group of small 
      non‑coding RNAs that regulate numerous signaling pathways involved in myocardial 
      I/R injury. The present study aimed to investigate whether miR‑451 protects 
      against cardiomyocyte anoxia/reoxygenation (A/R) injury by attenuating HMGB1 
      expression. Neonatal rat ventricular cardiomyocytes were prepared and then 
      subjected to A/R injury. The effect of upregulation or downregulation of miR‑451 
      on cell viability, apoptosis, superoxide dismutase (SOD) activity, and the 
      expression of cleaved‑caspase‑3 and HMGB1 were measured accordingly. A luciferase 
      assay was performed to further confirm whether miR‑451 can directly recognize the 
      3'‑untranslated region of HMGB1 in HEK293 cells. The expression of miR‑451 was 
      significantly decreased in the cardiomyocytes during A/R, and upregulation of 
      miR‑451 led to increased miR‑451 expression (P<0.05). Upregulation of miR‑451 
      significantly attenuated the loss of cardiomyocyte viability (P<0.05) and 
      increased the intracellular levels of SOD during A/R (P<0.05). Furthermore, 
      upregulation of miR‑451 significantly decreased the apoptosis of cardiomyocytes 
      during A/R (P<0.05). The HMGB1 mRNA and protein expression levels were 
      significantly downregulated in the Ad‑miR‑451 group compared with those in the 
      A/R group (P<0.05). In addition, upregulation of miR‑451 reduced its 
      translocation from the nucleus to the cytoplasm. The luciferase assay confirmed 
      that HMGB1 mRNA is a direct target of miR‑451 in cardiomyocytes. In conclusion, 
      the present study suggested that upregulation of miR‑451 could protect against 
      A/R‑induced cardiomyocyte injury by inhibiting HMGB1 expression.
FAU - Xie, Jing
AU  - Xie J
AD  - Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular 
      Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.
FAU - Hu, Xiaorong
AU  - Hu X
AD  - Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular 
      Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.
FAU - Yi, Chunfeng
AU  - Yi C
AD  - Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular 
      Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.
FAU - Hu, Gangying
AU  - Hu G
AD  - Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular 
      Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.
FAU - Zhou, Xiaoya
AU  - Zhou X
AD  - Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular 
      Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.
FAU - Jiang, Hong
AU  - Jiang H
AD  - Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular 
      Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20160426
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (HMGB1 Protein)
RN  - 0 (Hbp1 protein, rat)
RN  - 0 (MIRN451A microRNA, rat)
RN  - 0 (MicroRNAs)
SB  - IM
MH  - Animals
MH  - *Gene Expression Regulation
MH  - HEK293 Cells
MH  - HMGB1 Protein/*biosynthesis
MH  - Humans
MH  - MicroRNAs/*metabolism
MH  - Myocardial Reperfusion Injury/*metabolism/pathology/*prevention & control
MH  - Myocytes, Cardiac/*metabolism/pathology
MH  - Rats
EDAT- 2016/04/29 06:00
MHDA- 2017/02/17 06:00
CRDT- 2016/04/29 06:00
PHST- 2015/04/30 00:00 [received]
PHST- 2016/01/29 00:00 [accepted]
PHST- 2016/04/29 06:00 [entrez]
PHST- 2016/04/29 06:00 [pubmed]
PHST- 2017/02/17 06:00 [medline]
AID - 10.3892/mmr.2016.5192 [doi]
PST - ppublish
SO  - Mol Med Rep. 2016 Jun;13(6):5335-41. doi: 10.3892/mmr.2016.5192. Epub 2016 Apr 
      26.