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자료유형
학술저널
저자정보
Dai Qing (The First Affiliated Hospital of Xinjiang Medical University) Hong Yi (The First Affiliated Hospital of Xinjiang Medical University) Li Jie (The First Affiliated Hospital of Xinjiang Medical University)
저널정보
한국유전학회 Genes & Genomics Genes & Genomics Vol.43 No.9
발행연도
2021.9
수록면
1,003 - 1,009 (7page)
DOI
10.1007/s13258-021-01104-0

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Background The heart is one of the target organs vulnerable to sepsis. About 50% of sepsis patients will sufer from myocardial injury and cardiac dysfunction, which will aggravate the sepsis and afect its prognosis. Objectives Here, we attempt to investigate the function of long non coding RNA PVT1 in LPS-induced cardiac fbroblasts in vitro, and explore its potential mechanism. Methods The expression of PVT1 in LPS-induced cardiac fbroblasts was detected by qRT-PCR. CCK-8 assay, cell migration, qRT-PCR and western blotting analysis were applied to evaluating the efect of PVT1 knockdown on LPS-induced cardiac fbroblasts. The bioinformatics analysis and the rescue experiment were devoted to the underlying mechanism. Results PVT1 expression was up-regulated in LPS-induced cardiac fbroblasts. And knockdown of PVT1 inhibited cell viability and migration, alleviated infammation cytokines production of LPS-treated cardiac fbroblasts. The bioinformatics analysis predicted PVT1 negatively regulates miR-24 and KLF6 is a direct target of miR-24. Conclusions In a word, we observed PVT1 expression level was up-regulated in LPS- treated cardiac fbroblasts. PVT1 knockdown could alleviate LPS-induced biological behavior of cardiac fbroblasts through sponging miR-24 in vitro.

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