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

Biosci Rep. 2019 Jul 5;39(7):BSR20181613. doi: 10.1042/BSR20181613. Print 2019 Jul 31.


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.

Keywords: Inflammation; Myocardial ischemia-reperfusion injury; NF-κB; PLCE1.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

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


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