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Int J Clin Exp Pathol 2013;6(2):224-229

Original Article
Involvement of GMRP1, a novel mediator of Akt
pathway, in brain damage after intracerebral

Mingzhe Zheng, Hongda Zhu, Ye Gong, Daijun Wang, Qing Xie, Hailiang Tang, Zhihong Yang, Bin Lu,
Xiancheng Chen, Xuanchun Wang

Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China; Department of Endocrinology,
Huashan Hospital, Fudan University, Shanghai, China. *These authors contribute equally to this work.

Received September 12, 2012; Accepted November 20, 2012; Epub January 15, 2013; Published February 1,

Abstract: GMRP1, also known as BTBD10, has been reported to inhibit apoptosis of neuronal and islet beta cells
via Akt pathway. The present study attempted to investigate whether GMRP1 and its mediated Akt pathway were
involved in brain injury of rats after intracerebral hemorrhage (ICH). Rat models of ICH had been established successfully.
Western blotting was used to investigate the levels of GMRP1 protein in caudate nuclei tissues of hemorrhagic
and contralateral sides at 6 h, day 1, day 3, day 5, day 7 after ICH. Phosphorylation of Akt was determined in
caudate nuclei mentioned above. TUNEL assay was used to measure the cell apoptosis. GMRP1 protein levels, as
well as phosphorylations of Akt, significantly decreased in caudate nuclei of hemorrhagic side, compared with those
of contralateral side at day 1, day 3 after ICH. Enhanced cell apoptosis was observed in hemorrhagic side by TUNEL
assay. We presented here evidence that decreased GMRP1-mediated Akt pathway contributed to cell apoptosis in
hemorrhagic side, suggesting that GMRP1 played an important role in brain damage after ICH. (IJCEP1209006).

Keywords: GMRP1, intracerebral hemorrhage, apoptosis, Akt

Address all correspondence to:
Dr. Ye Gong
Department of Neurosurgery, Huashan Hospital
Fudan University, Shanghai, China.
E-mail: yyeegong@yahoo.com.cn;

Dr. Xuanchun Wang
Department of Endocrinology, Huashan Hospital
Fudan University, 12 Middle Wurumuqi Road
Shanghai, 200040, China.
Phone: +86 021-52889999; Fax: +86 021-52885325
E-mail: wangxch@fudan.edu.cn