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Published on: May 21, 2018
MicroRNA-223-3p/NLRP3 axis attenuates LPS-induced sepsis-like myocardial dysfunction by suppressing cardiomyocyte
Bixue Zhang1,2, Xin Li3, Qianqian Xu3
1Sixth Affiliated Hospital, Department of Cardiovascular Medicine, Xinjiang Medical University, Xinjiang Uygur Autonomous Region, Urumqi, 830054, China.
Background:
Sepsis-induced cardiomyopathy (SIC), a life-threatening complication of sepsis that is characterized by myocardial inflammation and cardiomyocyte death, remains a critical clinical challenge. MicroRNA (miRNA) is involved in the development of SIC. However, the roles and underlying mechanisms of miR-223-3p and pyroptosis in SIC remain unclear.
Methods And Results:
In vitro and in vivo LPS-induced sepsis-like myocardial dysfunction (SLMD) models were established in order to partially represent SIC. Assessments via CCK-8 assay, flow cytometry, qRT-PCR, Western blotting, immunofluorescence, histological staining, and transmission electron microscopy revealed that miR-223-3p overexpression significantly increased cardiomyocyte viability, reduced the marker levels of pyroptosis, improved cardiac function, and alleviated myocardial injury. In contrast, miR-223 knockout (KO) decreased cardiomyocyte viability, increased the marker levels of pyroptosis, aggravated heart failure, and induced cardiac damage. Mechanistically, miR-223-3p suppressed LPS-induced NLRP3 inflammasome activation and inhibited the LPS-induced interaction between caspase-1 and gasdermin D. Notably, upon treatment with NLRP3 siRNA or a GSDMD-targeting pyroptosis inhibitor disulfiram, miR-223-3p failed to exert additional protective effects against SLMD.
Conclusions:
These findings demonstrate that miR-223-3p attenuates LPS-Induced SLMD by inhibiting the NLRP3 inflammasome and cardiomyocyte pyroptosis.