Mechanism And Function Of Tisp40in Inflammatory Response After Myocardial Infarction

Objective: To investigate the mechanism and function of Tisp40in inflammatoryresponse after myocardial infarction.Methods: Wild type C57BL/6and cardiac specific Tisp40knock out male mice,were randomLy divided into MI and Sham group, coronary artery ligation (CAL)models or thoracotomy without CAL were established separately. After1week,echocardiography, HE staining, Real-time PCR, Western blot were used in all groups,and cardiac function, infarct size, indicators and expression of proteins ininflammatory response were evaluated, and compared between WT MI and KO MIgroups.Results:1week after CAL models were established, echocardiography shows thecardiac function of KO MI mice was significantly better than that of WT MI mice(LVEdD P＜0.05, LVEsD P＜0.05, FS P＜0.01), HE staining shows the infarct size ofKO MI mice was significantly smaller than that of WT MI mice (P＜0.05), Real-timePCR shows the indicators in inflammatory response of KO MI mice was significantlyless than that of WT MI mice (IL-1P＜0.01, IL-6P＜0.05, TNF-α P＜0.05), Westernblot shows the expression of proteins in inflammatory response of KO MI mice was significantly lower than that of WT MI mice (P-IκBα P＜0.001, P-NFκB P＜0.01).Conclusion: Inflammatory response was enhanced in WT mice groupafter myocardial infarction, which suggested the crucial role of inflammation inmyocardial infarction. Inflammatory response and cardiac function in KO mice groupwas weaker than that in WT mice group after myocardial infarction, these findingsindicated that Tisp40may play an important role in enhancing the inflammatoryresponse after myocardial infarction, which ultimately leads to the deteriorationof cardiac function.