β-Arrestin Prevents Cell Apoptosis Through Pro-Apoptotic ERK1/2 and p38 MAPKs and Anti-Apoptotic Akt Pathways
Document Type
Article
Publication Date
9-1-2012
Description
Our previous studies have shown that β-arrestin 2 plays an anti-apoptotic effect. However, the mechanisms by which β-arrestin contribute to anti-apoptotic role remain unclear. In this study, we show that a deficiency of either β-arrestin 1 or β-arrestin 2 significantly increases serum deprivation (SD)-induced percentage of apoptotic cells. β-arrestin 2 deficient-induced apoptosis was inhibited by transfection with β-arrestin 2 full-length plasmid, revealing that SD-induced apoptosis is dependent on β-arrestin 2. Furthermore, in the absence of either β-arrestin 1 or β-arrestin 2 significantly enhances SD-induced the level of pro-apoptotic proteins, including cleaved caspase-3, extracellular-signal regulated kinase 1/2 (ERK1/2) and p38, members of mitogen-activated protein kinases (MAPKs). In addition, a deficiency of either β-arrestin 1 or β-arrestin 2 inhibits phosphorylation of Akt. The SD-induced changes in cleaved caspase-3, ERK1/2 and p38 MAPKs, Akt, and apoptotic cell numbers could be blocked by double knockout of β-arrestin 1/2. Our study thus demonstrates that β-arrestin inhibits cell apoptosis through pro-apoptotic ERK1/2 and p38 MAPKs and anti-apoptotic Akt signaling pathways.
Citation Information
Yang, Xiaohua; Zhou, Gengyin; Ren, Tao; Li, Hui; Zhang, Yanjun; Yin, Deling; Qian, Haixin; and Li, Qinchuan. 2012. β-Arrestin Prevents Cell Apoptosis Through Pro-Apoptotic ERK1/2 and p38 MAPKs and Anti-Apoptotic Akt Pathways. Apoptosis. Vol.17(9). 1019-1026. https://doi.org/10.1007/s10495-012-0741-2 PMID: 22699970 ISSN: 1360-8185