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

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

WenHua Li  1 Yong Li  1 Ying Chu  2 WeiMin Wu  3 QiuHua Yu  3 XiaoBo Zhu  3 Qiang Wang  4

Affiliations

  • 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 qiangwwujin@163.com.

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.

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

© 2019 The Author(s).

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