PLCE1 Promotes Myocardial Ischemia-Reperfusion Injury in H/R H9c2 Cells and I/R Rats by Promoting Inflammation
- 1 Department of Cardiology, Wujin People’s Hospital of Changzhou, Changzhou 213017, China.
- 2 Central Laboratory, Wujin People’s Hospital of Changzhou, Changzhou 213017, China.
- 3 Department of Cardio-Thoracic, Wujin People’s Hospital of Changzhou, Changzhou 213017, China.
- 4 Department of Cardio-Thoracic, Wujin People’s Hospital of Changzhou, Changzhou 213017, China email@example.com.
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.