PMID- 36086866
OWN - NLM
STAT- MEDLINE
DCOM- 20221222
LR  - 20221222
IS  - 1099-0461 (Electronic)
IS  - 1095-6670 (Linking)
VI  - 36
IP  - 12
DP  - 2022 Dec
TI  - miR-208 inhibits myocardial tissues apoptosis in mice with acute myocardial 
      infarction by targeting inhibition of PDCD4.
PG  - e23202
LID - 10.1002/jbt.23202 [doi]
AB  - This article aimed to investigate the role of miR-208 in the apoptosis of 
      myocardial tissues in acute myocardial infarction (AMI) mice. The AMI mouse model 
      was constructed. Then, miR-208 expression in AMI mice was regulated by 
      transfection. The mouse myocardial tissues were subject to hematoxylin-eosin (HE) 
      staining, TUNEL assay, and immunofluorescence analysis. H9c2 cell transfection 
      and hypoxia induction were then completed, and cell apoptosis and cytokine levels 
      were tested. Additionally, RNA pull-down and dual luciferase reporter gene assays 
      were conducted for exploring the relation of miR-208 with programmed cell death 4 
      (PDCD4). Additionally, fluorescence in situ hybridization (FISH) was conducted 
      for investigating miR-208 and PDCD4 colocalization within H9c2 cells. AMI mice 
      had severe damage, apoptosis, decreased miR-208 expression, increased IL-1beta, 
      IL-6, IL-8 levels, whereas reduced IL-10 level within myocardial tissues. H9c2 
      cells under hypoxia induction exhibited decreased miR-208 expression, promoted 
      apoptosis, increased protein expression of Bax and cleaved-caspase-3, decreased 
      protein expression of Bcl-2 and caspase-3, elevated IL-1beta, IL-6, IL-8 levels and 
      decreased IL-10 level. miR-208 upregulation alleviated the damage and apoptosis 
      of myocardial tissues in AMI mice. AMI mice with miR-208 upregulation showed 
      decreased expression of Bax and cleaved-caspase-3, increased expression of Bcl-2 
      and caspase-3, reduced levels of IL-1beta, IL-6, IL-8, whereas an increased level of 
      IL-10. miR-208 showed direct inhibition of PDCD4. PDCD4 and miR-208 were mainly 
      co-expressed in the cytoplasm. The upregulated PDCD4 expression abolished 
      miR-208's suppression of H9c2 cell apoptosis induced by hypoxia. Besides this, 
      miR-208 inhibited myocardial tissue apoptosis in AMI mice by inhibiting PDCD4 
      expression.
CI  - (c) 2022 Wiley Periodicals LLC.
FAU - Wang, Qiang
AU  - Wang Q
AUID- ORCID: 0000-0002-2719-8809
AD  - Department of Cardio-thoracic Surgery, Wujin Hospital Affiliated with Jiangsu 
      University, The Wujin Clinical College of Xuzhou Medical University, Changzhou, 
      People's Republic of China.
FAU - Zhou, Huxiang
AU  - Zhou H
AD  - Medical College of Jiangsu University, Zhenjiang, People's Republic of China.
FAU - Zhu, Xiaobo
AU  - Zhu X
AD  - Department of Cardio-thoracic Surgery, Wujin Hospital Affiliated with Jiangsu 
      University, The Wujin Clinical College of Xuzhou Medical University, Changzhou, 
      People's Republic of China.
FAU - Jiang, Feng
AU  - Jiang F
AD  - Department of Cardio-thoracic Surgery, Wujin Hospital Affiliated with Jiangsu 
      University, The Wujin Clinical College of Xuzhou Medical University, Changzhou, 
      People's Republic of China.
FAU - Yu, Qiuhua
AU  - Yu Q
AD  - Department of Cardio-thoracic Surgery, Wujin Hospital Affiliated with Jiangsu 
      University, The Wujin Clinical College of Xuzhou Medical University, Changzhou, 
      People's Republic of China.
FAU - Zhang, Junjie
AU  - Zhang J
AD  - Department of Cardio-thoracic Surgery, Wujin Hospital Affiliated with Jiangsu 
      University, The Wujin Clinical College of Xuzhou Medical University, Changzhou, 
      People's Republic of China.
FAU - Ji, Yaxiang
AU  - Ji Y
AD  - Department of Cardiac Ultrasound, Wujin Hospital Affiliated with Jiangsu 
      University, The Wujin Clinical College of Xuzhou Medical University, Changzhou, 
      People's Republic of China.
LA  - eng
GR  - H2019080/This study was supported by Scientific Research Project of Jiangsu 
      Health and Health Commission/
GR  - LGY2018018/The Fifth "333 Project" Talent Training Project in Jiangsu Province/
GR  - WS2019014/Wujin District Science and Technology Bureau Project/
GR  - WS201917/Wujin District Science and Technology Bureau Project/
PT  - Journal Article
DEP - 20220909
PL  - United States
TA  - J Biochem Mol Toxicol
JT  - Journal of biochemical and molecular toxicology
JID - 9717231
RN  - 0 (Apoptosis Regulatory Proteins)
RN  - 0 (bcl-2-Associated X Protein)
RN  - EC 3.4.22.- (Caspase 3)
RN  - 130068-27-8 (Interleukin-10)
RN  - 0 (Interleukin-6)
RN  - 0 (Interleukin-8)
RN  - 0 (MicroRNAs)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (Pdcd4 protein, mouse)
RN  - 0 (Mirn208 microRNA, mouse)
SB  - IM
MH  - Animals
MH  - Mice
MH  - Apoptosis/genetics
MH  - *Apoptosis Regulatory Proteins/genetics/metabolism
MH  - bcl-2-Associated X Protein/metabolism
MH  - Caspase 3/metabolism
MH  - Hypoxia/metabolism
MH  - In Situ Hybridization, Fluorescence
MH  - Interleukin-10/metabolism
MH  - Interleukin-6/metabolism
MH  - Interleukin-8/metabolism
MH  - *MicroRNAs/metabolism
MH  - *Myocardial Infarction/genetics/metabolism
MH  - Myocytes, Cardiac/metabolism
MH  - Proto-Oncogene Proteins c-bcl-2/metabolism
OTO - NOTNLM
OT  - AMI
OT  - PDCD4
OT  - apoptosis
OT  - hypoxia
OT  - miR-208
EDAT- 2022/09/11 06:00
MHDA- 2022/12/17 06:00
CRDT- 2022/09/10 02:42
PHST- 2022/07/03 00:00 [revised]
PHST- 2021/11/12 00:00 [received]
PHST- 2022/08/16 00:00 [accepted]
PHST- 2022/09/11 06:00 [pubmed]
PHST- 2022/12/17 06:00 [medline]
PHST- 2022/09/10 02:42 [entrez]
AID - 10.1002/jbt.23202 [doi]
PST - ppublish
SO  - J Biochem Mol Toxicol. 2022 Dec;36(12):e23202. doi: 10.1002/jbt.23202. Epub 2022 
      Sep 9.