Lnc-PXMP4-2-4 alleviates myocardial cell damage by activating the JAK2/STAT3 signaling pathway

Hong Zhang; Qinlin Guo; Guiju Feng; Xin Shen; Xinxin Feng; Yi Guo; Shouyan Wang; Xia Zhong

doi:10.1016/j.heliyon.2023.e18649

Lnc-PXMP4-2-4 alleviates myocardial cell damage by activating the JAK2/STAT3 signaling pathway

Heliyon. 2023 Jul 26;9(8):e18649. doi: 10.1016/j.heliyon.2023.e18649. eCollection 2023 Aug.

Authors

Hong Zhang¹, Qinlin Guo², Guiju Feng¹, Xin Shen¹, Xinxin Feng³, Yi Guo¹, Shouyan Wang¹, Xia Zhong¹

Affiliations

¹ Department of General Practice, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, People's Republic of China.
² Department of Endocrine, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, 250021, People's Republic of China.
³ Department of Pediatric Cardiology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, 250012, People's Republic of China.

Abstract

Purpose: The aim of this study was to investigate the protective effect of long non-coding lnc-PXMP4-2-4 on myocardial cell damage caused by acute myocardial infarction (AMI).

Methods: Peripheral blood mononuclear cells (PBMC) were collected from 24 patients with AMI on the day of admission, the first day after percutaneous coronary intervention (PCI) and the third day after surgery, and 24 patients with clinical control group. Real-time quantitative PCR(QRT-PCR) was used to detect the expression of related genes. Then in human cardiomyocytes (AC16), Cell Counting Kit-8 (CCK-8) was used to determine cell viability, lactate dehydrogenase release assay (LDH) was used to determine the release of lactate dehydrogenase, PCR was used to detect the expression of genes, cell death was detected by flow cytometry, and the expression of related proteins was measured by Western blot. The effect of lnc-PXMP4-2-4 was further studied by silencing and overexpressing lnc-PXMP4-2-4.

Results: Compared with clinical control group, the expression of lnc-PXMP4-2-4 in PBMC of AMI patients was significantly higher than it. Compared with pre-operation, the expression of lnc-PXMP4-2-4 was significantly up-regulated on day 1 after PCI, and recovered to pre-operation level on day 3 after surgery. In AC16 cells, lnc-PXMP4-2-4 inhibited the proliferation of AC16, promoted the release of LDH and increased cell death, aggravated the cardiomyocyte injury caused by H₂O₂, and inhibited the expression of JAK2 and STAT3 mRNA and protein. The up-regulation of lnc-PXMP-4-2-4 had the opposite effect. In addition, the inhibition of the signal pathway by JAK2/STAT3 pathway inhibitor AG490 partially weakened the enhanced viability of AC16 cells, decreased LDH release and apoptosis induced by lnc-PXMP4-2-4 overexpression, increased Bcl-2 expression and down-regulated Bax expression.

Conclusion: Therefore, we conclude that lnc-PXMP4-2-4 protects cardiomyocytes from injury by activating the JAK2/STAT3 signaling pathway.

Keywords: Acute myocardial infarction; Cell damage; JAK2/STAT3; lnc-PXMP4-2-4.