Volume 40, Issue 4 pp. 339-348

Glucose-regulated protein 75 suppresses apoptosis induced by glucose deprivation in PC12 cells through inhibition of Bax conformational change

Ling Yang

Ling Yang

Department of Cellular and Genetic Medicine, Shanghai Medical College, Fudan University, Shanghai 200032, China

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Xiaoyu Liu

Xiaoyu Liu

Department of Cellular and Genetic Medicine, Shanghai Medical College, Fudan University, Shanghai 200032, China

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Jinyu Hao

Jinyu Hao

Department of Cellular and Genetic Medicine, Shanghai Medical College, Fudan University, Shanghai 200032, China

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Yunlong Yang

Yunlong Yang

Department of Cellular and Genetic Medicine, Shanghai Medical College, Fudan University, Shanghai 200032, China

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Mingxia Zhao

Mingxia Zhao

Department of Cellular and Genetic Medicine, Shanghai Medical College, Fudan University, Shanghai 200032, China

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Ji Zuo

Ji Zuo

Department of Cellular and Genetic Medicine, Shanghai Medical College, Fudan University, Shanghai 200032, China

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Wen Liu

Corresponding Author

Wen Liu

Department of Cellular and Genetic Medicine, Shanghai Medical College, Fudan University, Shanghai 200032, China

*Corresponding author: Tel, 86-21-54237311; Fax, 86-21-54237091; e-mail, [email protected]Search for more papers by this author
First published: 21 April 2008
Citations: 3

This work was supported by a grant from the Specialized Research Fund for the Doctoral Program of Higher Education of China (No. 20050246079)

Abstract

Glucose-regulated protein 75 (Grp75) is an important molecular chaperone that belongs to the heat shock protein 70 family and resides predominantly in mitochondria. Grp75 can protect cells from glucose deprivation (GD) injury. However, the molecular mechanisms by which it carries out this function are unknown. Here we report that Grp75 could delay the release of cytochrome c and reduce apoptosis induced by GD, and we also found that Grp75 could decrease Bax/Bcl-2 gene expression ratio and inhibit the conformational change of Bax during this process. In conclusion, these findings suggested that Grp75 overexpression was able to inhibit apoptosis induced by GD. Grp75 inhibited Bax conformational change to delay the release of cytochrome c, thus providing protection to PC12 cell which was used primarily as a neuron model against GD toxicity.

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