miR‐17 targets tissue inhibitor of metalloproteinase 1 and 2 to modulate cardiac matrix remodeling

We aimed to investigate the role of miR‐17 in cardiac matrix remodeling following myocardial infarction (MI). Using real‐time PCR, we quantified endogenous miR‐17 in infarcted mouse hearts. Compared with related microRNAs, miR‐17 was up‐regulated most dramatically: 3.7‐fold and 2.4‐fold in the infar...

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Bibliographic Details
Published in:The FASEB journal 2013-10, Vol.27 (10), p.4254-4265
Main Authors: Li, Shu‐Hong, Guo, Jian, Wu, Jun, Sun, Zhuo, Han, Mihan, Shan, Sze Wan, Deng, Zhaoqun, Yang, Burton B., Weisel, Richard D., Li, Ren‐Ke
Format: Article
Language:English
Subjects:
Animals
Gene Expression Regulation - physiology
HEK293 Cells
Humans
Mice
Mice, Inbred C57BL
Mice, Transgenic
MicroRNAs - genetics
MicroRNAs - metabolism
MMP
myocardial infarction
Myocardial Infarction - metabolism
Myocardium - metabolism
Oligonucleotides
TIMP1
TIMP2
Tissue Inhibitor of Metalloproteinase-1 - genetics
Tissue Inhibitor of Metalloproteinase-1 - metabolism
Tissue Inhibitor of Metalloproteinase-2 - genetics
Tissue Inhibitor of Metalloproteinase-2 - metabolism
Ventricular Remodeling
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Summary:We aimed to investigate the role of miR‐17 in cardiac matrix remodeling following myocardial infarction (MI). Using real‐time PCR, we quantified endogenous miR‐17 in infarcted mouse hearts. Compared with related microRNAs, miR‐17 was up‐regulated most dramatically: 3.7‐fold and 2.4‐fold in the infarct region 3 and 7 d post‐MI, respectively, and 2.4‐fold in the border zone at d 3 compared to sham control (P
ISSN:0892-6638
1530-6860
DOI:10.1096/fj.13-231688