Increased Dp71 in ischemia-reperfusion injured rat heart exerts anti-apoptotic role via enhancing Bcl-2. (December 2022)

• Record Type: Journal Article
• Authors: Zhu, Yaxi; Zhao, Shuai; Xiao, Lan; Wu, Yongbin; Wang, Qianlu; He, Shijun; Tan, Sichuang; Tan, Sipin
• Is Part Of: Tissue & cell. Volume 79(2022)
• Publication Date: 2022-12
• Subjects: Dp71 -- Ischemia-reperfusion injury -- Bcl-2 -- Apoptosis; Cytology -- Periodicals; 571.5
• DOI: 10.1016/j.tice.2022.101951
• Languages: English
• ISSNs: 0040-8166

Abstract

Abstract: For the first time, increased Dp71 in ischemia-reperfusion injured rat heart were identified, both Dp71 mRNA and protein reached its peak expression 8 h after reperfusion. In H2 O2 stimulated H9c2 cells, Dp71 mRNA and protein gradually increased and reached a peak at 16 h. Enhanced Dp71 in H9c2 could resist H2 O2 -induced cell apoptosis, while Dp71 depletion accelerated the apoptosis induced by H2 O2. Enhanced Bcl-2 expression and Bcl-2∕Bax protein expression ratio was identified in Dp71 overexpressed H9c2 cells, while knocking down Dp71 significantly decreased the Bcl-2 and Bcl-2∕Bax protein expression ratio. Increased Dp71 can accelerate FAK and p65 phosphorylation, which finally resulted in enhanced Bcl-2 expression and explains the highly possible cardiac protection role of Dp71. Highlights: In creased DP71 was identified in ischemia-reperfusion injured rat heart and H2 O2 stimulated H9c2 cell. Enhanced DP71 in H9c2 can resist H2 O2 -induced cell apoptosis while Dp71 depletion accelerated the apoptosis induced by H2 O2 . Enhanced Bcl-2 expression indicates the cardiac protection role of DP71 derived by acceleration of FAK&p65 phosphorrylation.