PLCE1 promotes myocardial ischemia-reperfusion injury in H/R H9c2 cells and I/R rats by promoting inflammation.

Abstract

Myocardial ischemia-reperfusion (I/R) injury is a major contributor to the morbidity and mortality associated with coronary artery disease. How to ensure the recovery of blood supply to ischemic myocardial tissue while avoiding or reducing I/R injury remains a critical problem in clinical practice. In the present study, we examined the function of phospholipase C ϵ-1 (PLCE1) by an H9c2 H/R (H/R, hypoxia-reoxygenation) model and a rat myocardial I/R injury model. The expression of PLCE1 and its effect on I/R injury-induced inflammatory response as well as its possible underlying mechanism were investigated. Our results have shown that PLCE1 was progressively increased along with the increase in hypoxia time in the H/R H9c2 and HL-1 cells. In myocardial I/R rats, PLCE1 presented a low expression level in the sham group, however, it was increased sharply in the I/R group. Overexpression of PLCE1 promoted the expression of IL-6, TNF-α, and IL-1α, and decreased the expression of IL-10. Knockdown of PLCE1 decreased the expression of IL-6, TNF-α, and IL-1α, and increased the expression of IL-10. Furthermore, overexpression of PLCE1 increased the phosphorylation of p38, ERK1/2, and nuclear factor-κ B (NF-κB) P65 while knockdown of PLCE1 inhibited their phosphorylation. In conclusion, the present study provided evidence that PLCE1 was up-regulated in H/R H9c2 cell and I/R rat. Overexpression of PLCE1 promoted the inflammatoion via activation of the NF-κB signaling pathway.

• Authors: WenHua Li, Yong Li, Ying Chu, WeiMin Wu, QiuHua Yu, XiaoBo Zhu, Qiang Wang
• Journal: Bioscience reports (Biosci Rep) Vol. 39 Issue 7 (07 31 2019) ISSN: 1573-4935 [Electronic] England
• PMID: 31217261 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: © 2019 The Author(s).

Chemical References

• Interleukin-1alpha
• Interleukin-6
• Tumor Necrosis Factor-alpha
• Interleukin-10
• p38 Mitogen-Activated Protein Kinases
• Phosphoinositide Phospholipase C
• phospholipase C epsilon

Topics

• Animals
• Cell Line
• Gene Expression Regulation (genetics)
• Gene Knockdown Techniques
• Humans
• Inflammation (genetics, pathology)
• Interleukin-10 (genetics)
• Interleukin-1alpha (genetics)
• Interleukin-6 (genetics)
• MAP Kinase Signaling System (genetics)
• Myocardial Ischemia (genetics, pathology)
• Phosphoinositide Phospholipase C (genetics)
• Phosphorylation (genetics)
• Rats
• Reperfusion Injury (genetics, pathology)
• Tumor Necrosis Factor-alpha (genetics)
• p38 Mitogen-Activated Protein Kinases (genetics)