2. Academic Validation
  3. Poly(ADP-ribose) polymerase inhibitor PJ34 protects against UVA-induced oxidative damage in corneal endothelium

Poly(ADP-ribose) polymerase inhibitor PJ34 protects against UVA-induced oxidative damage in corneal endothelium

  • Apoptosis. 2021 Dec;26(11-12):600-611. doi: 10.1007/s10495-021-01690-0.
Xin Wang 1 2,  Chunxiao Dong 1,  Qingjun Zhou 1,  Haoyun Duan 1,  Dulei Zou 1,  Yajie Gong 1,  Bochao Ma 1,  Zongyi Li 3,  Weiyun Shi 4 5
Affiliations

Affiliations

  • 1 State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong First Medical University & Shandong Academy of Medical Sciences, 5 Yan'erdao Road, Qingdao, 266071, China.
  • 2 Eye Hospital of Shandong First Medical University, Jinan, China.
  • 3 State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong First Medical University & Shandong Academy of Medical Sciences, 5 Yan'erdao Road, Qingdao, 266071, China. lizongyi119@163.com.
  • 4 State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong First Medical University & Shandong Academy of Medical Sciences, 5 Yan'erdao Road, Qingdao, 266071, China. weiyunshi@163.com.
  • 5 Eye Hospital of Shandong First Medical University, Jinan, China. weiyunshi@163.com.
PMID: 34581992 DOI: 10.1007/s10495-021-01690-0
Abstract

Fuchs endothelial corneal dystrophy (FECD) is one of the main causes for corneal endothelial blindness, which is characterized by the progressive decline of corneal endothelial cells. Poly (ADP-ribose) polymerase (PARP) was reported to be involved in cell death and Apoptosis of several diseases. However, the role of PARP1 in the progression of FECD remains elusive. In the present study, we reported that UVA irradiation caused the corneal endothelial damage and corneal edema in mice, which was accompanied with the elevated activity of PARP1 and PAR. The PARP1 Inhibitor PJ34 resolved the corneal edema and protected corneal endothelium from UVA-induced oxidative damage, mitochondrial dysfunction, and cell Apoptosis. Mechanistically, PARP1 inhibition exerted its anti-apoptotic effects through downregulation of the phosphorylation levels of JNK1/2 and p38 MAPK and subsequently the increase of MKP-1. Our results suggest that PARP1 inhibition protects corneal endothelium from UVA-induced oxidative damage, which provides a potential alternative strategy for the therapy of FECD.

Keywords

Apoptosis; Corneal endothelium; Fuchs endothelial corneal dystrophy; Oxidate damage; PARP.

Figures
Products
  • Cat. No.
    Product Name
    Description
    Target
    Research Area
  • HY-13688A
    98.11%, PARP Inhibitor