Polish Journal of Pathology
eISSN: 2084-9869
ISSN: 1233-9687
Polish Journal of Pathology
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without publication fees
2/2025
vol. 76
 
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abstract:
Original paper

miR-21 regulates LPS-induced apoptosis and inflammatory injury in rat cardiomyocytes by targeting PLD1 and STAT3

Rui Chen
1
,
Wei Xiong
1
,
Ruiying Liu
1
,
Sai Wan
1
,
Tao Huang
1
,
Jiajing Ai
1
,
Lingjing Ye
1
,
Qingping He
2

  1. Department of Emergency, Yingtan People’s Hospital, Yingtan, Jiangxi, China
  2. Department of Rehabilitation Medicine, Yingtan People’s Hospital, Yingtan, Jiangxi, China
Pol J Pathol2025; 76 (2): 131-140
DOI: https://doi.org/10.5114/pjp.2025.153974
Online publish date: 2025/09/22
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This study aims to elucidate the role and molecular mechanism of microRNA-21 (miR-21) in LPS-induced inflammatory injury in H9c2 cardiomyocytes.

H9c2 cardiomyocytes were treated with lipopolysaccharide (LPS) to establish an in vitro model. The expression of miR-21 was quantified using RT-qPCR, while protein levels were assessed via Western blot analysis. The impact of miR-21 on inflamma­tory response, cell proliferation, and apoptosis in LPS-treated H9c2 cells was evalu­ated using ELISA, CCK-8/EdU assays, and flow cytometry. TargetScan predictions and dual-luciferase reporter assays were employed to identify potential miR-21 tar­gets. The regulatory effects of miR-21 on inflammation, proliferation, and apop­tosis in cells were further examined following transfection with phospholipase D1 (PLD1) overexpression constructs or signal transducer and activator of transcription 3 (STAT3) activation. The expression levels of miR-21, PLD1, and p-STAT3 were significantly elevated in LPS-treated H9c2 cells. Knockdown of miR-21 markedly inhibited the LPS-induced inflammatory response, enhanced cell proliferation, and reduced apoptosis in H9c2 cells. PLD1 and STAT3 were confirmed as direct targets of miR-21. Overexpression of PLD1 or activation of STAT3 significantly reversed the protective effects of miR-21 downregulation in LPS-treated H9c2 cells. Downregu­lation of miR-21 protects cardiomyocytes against LPS-induced inflammatory injury and apoptosis by inhibiting PLD1 expression and STAT3 phosphorylation.
keywords:

HmiR-21, PLD1, STAT3, sepsis, myocardial injury
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