Glycogen synthase kinase-3&#946; facilitates cell apoptosis induced by high fluence low-power laser irradiation through acceleration of Bax translocation

Lei Huang; Shengnan Wu; Da Xing

doi:10.1117/12.874138

17 February 2011 Glycogen synthase kinase-3β facilitates cell apoptosis induced by high fluence low-power laser irradiation through acceleration of Bax translocation

Lei Huang, Shengnan Wu, Da Xing

Author Affiliations +

Proceedings Volume 7887, Mechanisms for Low-Light Therapy VI; 788708 (2011) https://doi.org/10.1117/12.874138
Event: SPIE BiOS, 2011, San Francisco, California, United States

Abstract

Glycogen synthase kinase-3β (GSK-3β) is a critical activator of cell apoptosis induced by a diverse array of insults. However, the effects of GSK-3β on the human lung adenocarcinoma cell (ASTC-a-1) apoptosis induced by high fluence low-power laser irradiation (HF-LPLI) are not clear. Here, we showed that GSK-3β was constantly translocated from cytoplasm to nucleus and activated during HF-LPLI-induced cell apoptosis. In addition, we found that co-overexpression of YFP-GSK-3β and CFP-Bax in ASTC-a-1 cells accelerated both Bax translocations to mitochondria and cell apoptosis, compared to the cells expressed CFP-Bax only under HF-LPLI treatment, indicating that GSK-3β facilitated ASTC-a-1 cells apoptosis through acceleration mitochondrial translocation of Bax. Our results demonstrate that GSK-3β exerts some of its pro-apoptotic effects in ASTC-a-1 cells by regulating the mitochondrial localization of Bax, a key component of the intrinsic apoptotic cascade.

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Lei Huang, Shengnan Wu, and Da Xing "Glycogen synthase kinase-3β facilitates cell apoptosis induced by high fluence low-power laser irradiation through acceleration of Bax translocation", Proc. SPIE 7887, Mechanisms for Low-Light Therapy VI, 788708 (17 February 2011); https://doi.org/10.1117/12.874138

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