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LncRNA H19 Inhibits the Progression of Sepsis-Induced Myocardial Injury via Regulation of the miR-93-5p/SORBS2 Axis

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Abstract

Sepsis is an infectious disease that seriously endangers human health. It usually leads to myocardial injury which seriously endangers to the health of human beings. H19 has been confirmed to play key roles in various diseases, including sepsis. However, its function in the progression of sepsis-induced myocardial injury remains largely unknown. H9C2 cells were treated with lipopolysaccharide (LPS) to mimic sepsis-induced myocardial injury in vitro. Cell proliferation and apoptosis were detected by MTT assay and flow cytometry, respectively. In addition, gene and protein expression levels in H9C2 cells were measured by quantitative real-time PCR (qRT-PCR) and Western blotting. The levels of inflammatory cytokines in H9C2 cell supernatants were tested by ELISA. JC-1 staining was performed to observe the mitochondrial membrane potential level in H9C2 cells. H19 and SORBS2 were downregulated in H9C2 cells following LPS treatment, while miR-93-5p was upregulated. Moreover, LPS-induced cell growth inhibition and mitochondrial damage were significantly reversed by overexpression of H19. In addition, H19 upregulation notably suppressed LPS-induced inflammatory responses in H9C2 cells. Moreover, H19 sponged miR-93-5p to promote SORBS2 expression. Overall, H19 suppressed sepsis-induced myocardial injury via regulation of the miR-93-5p/SORBS2 axis. H19 attenuated the development of sepsis-induced myocardial injury in vitro via modulation of the miR-93-5p/SORBS2 axis. Thus, H19 could serve as a potential target for the treatment of sepsis-induced myocardial injury.

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All data generated or analysed during this study are included in this published article.

Abbreviations

SORBS2:

sorbin and SH3 domain-containing 3

MiR-93-5p:

microRNA-93-5p

LncRNA H19:

long noncoding RNA H19

FBS:

foetal bovine serum

MTT:

3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide

DMSO:

dimethyl sulfoxide

cTnT:

cardiac troponin T

TNF-α:

tumour necrosis factor-α

IL-1β:

interleukin-1β

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Funding

We thank the support of the funding obtained from Chenzhou Bureau of Science and Technology (ZDYF2020095 and ZDYF201941).

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Guarantor of integrity of the entire study: Bin Shan, Liang-Xian Luo.

Study concepts: Bin Shan.

Study design: Bin Shan, Liang-Xian Luo.

Definition of intellectual content: Bin Shan, Jia-Yan Li.

Literature research: Bin Shan, Jia-Yan Li, Ya-Jiang Liu.

Experimental studies: Ya-Jiang Liu, Xiao-Bin Tang, Zheng Zhou.

Data acquisition: Bin Shan, Zheng Zhou.

Data analysis: Xiao-Bin Tang, Zheng Zhou.

Statistical analysis: Xiao-Bin Tang, Zheng Zhou.

Manuscript preparation: Bin Shan, Liang-Xian Luo.

Manuscript editing: Bin Shan, Liang-Xian Luo.

Manuscript review: Bin Shan, Liang-Xian Luo.

All the authors approved for the final version.

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Correspondence to Liang-Xian Luo.

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Shan, B., Li, JY., Liu, YJ. et al. LncRNA H19 Inhibits the Progression of Sepsis-Induced Myocardial Injury via Regulation of the miR-93-5p/SORBS2 Axis. Inflammation 44, 344–357 (2021). https://doi.org/10.1007/s10753-020-01340-8

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