Abstract:
MicroRNAs (miRNAs) are considered as a small non-coding RNA which
regulateexpression of gene by preventing the translation including destruction of specific
mRNA.Acute myocardial infarction (AMI) is characterized by inflammation,
cardiomyocyteapoptosis, and cardiac necrosis that may develop heart failure. Necroptosis
is a form ofregulated necrosis and is dependent on a signaling pathway involving receptor
interactingprotein kinase (RIPK). Fas-associated protein with death domain (FADD) is a
negativeregulator for necroptosis. MicroRNAs play a critical role in the pathogenesis
ofcardiovascular diseases. 10 mice were randomly assigned into two groups: normal
controlgroup and induction group by s.c injection of isoprenaline (100 mg/kg). Heart
injury wasevaluated through the histological examination in heart tissue, in addition to
thebiochemical assessment of troponin I. The levels of miRNA-103 in heart tissues
weredetermined using based miRNA quantitative real-time polymerase chain reactions
(qRT-PCRs). The following parameters were investigated for studying the
possiblemechanisms of miRNA-103 in necrosis: FADD, RIPK and IL-6 (Interleukine-6).
Theresults revealed that in AMI group miRNA 103 was significantly elevated while
theexpression level of FADD was decreased, moreover RIPK and IL-6 were
significantlyincreased. In exploring the molecular mechanism of miRNA 103 in AMI,
The presentstudy provides new evidence showing that miRNA 103 up regulation through
targetingFADD, resulting loss of FADD leads to resistance to apoptosis and cells
undergonecroptosis instead. In conclusion, miR-103 might be considered a novel
potentialbiomarkers for AMI and its modulation provide a new approach for preventing
AMI.
