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Role And Mechanism Of Interleukin-15 In Myocardial Injury After Acute Myocardial Infarction

Posted on:2021-03-03Degree:MasterType:Thesis
Country:ChinaCandidate:L GuoFull Text:PDF
GTID:2404330614968419Subject:Internal medicine (cardiovascular disease)
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Background:Inflammatory regulation after acute myocardial infarction is a hot topic in myocardial infarction research.Interleukin-15 is a recently discovered inflammatory cytokine and demonstrates a variety of biological effects.Clinical studies have found that the serum interleukin-15 concentration in patients with atherosclerosis is significantly higher than that in healthy people.This study investigated the role of interleukin-15 in myocardial injury after myocardial infarction in a mouse model.Interleukin-15 and interleukin-15α receptor gene knockout mice and primary cultured cell models were introduced to explore its mechanism of action.Methods and results:A mouse myocardial infarction model was established by permanent ligation of the anterior descending coronary artery,and heart samples were collected at different time points.The expressions of interleukin-15 and interleukin-15α receptors in infarcted and non-infarcted myocardium were detected by Western Blot.Increased expression of both interleukin-15 and its receptors were found in the infarcted area after myocardial infarction,especially at the acute phase,while the expression of interleukin-15 was low-expressed in non-infarcted myocardium.Hypoxia and serum deprivation significantly induced the expression of interleukin-15 and interleukin-15α receptors inprimary cultured cardiomyocytes.When comparing to the wild type controls,mice with interleukin-15 or interleukin-15α receptors deficiency demonstrated attenuated cardiomyocyte apoptosis,reduced infarct size and preserved cardiac function after myocardial infarction.Exogenous application of interleukin-15 cytokine promote the apoptosis of cultured mouse cardiomyocytes.Conclusion:After myocardial infarction,interleukin-15,which mainly produced by macrophages aggravates myocardial injury by promoting cardiomyocyte apoptosis.Interleukin-15 or interleukin-15α receptor deficiency reduced infarct size and preserved cardiac function after myocardial infarction.Intervention strategies through interleukin-15 or interleukin-15α receptor may be a new target for improving cardiac function after acute myocardial infarction.
Keywords/Search Tags:Interleukin-15, myocardial injury, apoptosis, inflammation, acute myocardial infarction
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