Adenosine A2A receptor deficiency prevents p38MAPK activation and apoptosis of mouse hippocampal cells in the chronic hypoxic-hypercapnia model

Author:

Ren Huiming1,Guo Xu1,Wang Xiaotong2,Cui Zhihui3

Affiliation:

1. Department of Rehabilitation Medicine, Hwa Mei Hospital, University of Chinese Academy of Sciences, China, Ningbo, Zhejiang, P.R. China

2. The Center of Rehabilitation & Neurology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China

3. Department of Rehabilitation, Ningbo College of Health Sciences, Ningbo, Zhejiang, P.R. China

Abstract

ABSTRACT This study aims to study the effects of adenosine A2A receptor (A2AR) on hippocampal cell apoptosis and the putative mechanisms in a mouse model of chronic hypoxic-hypercapnia. Wild-type (WT) or A2AR knockout (A2AR KO) mice were randomly divided into normal control (NC) groups and chronic hypoxic-hypercapnia (4HH) groups. Compared with their corresponding NC groups (WT-NC and KO-NC), the apoptosis index (AI), caspase-3 activity, Bax mRNA and P-p38 protein expression in the hippocampus of 4HH groups (WT-4HH and KO-4HH) were significantly increased, while Bcl2 mRNA expression was significantly decreased (P < 0.05). Moreover, A2AR deficiency significantly rescued the effect of chronic hypoxic-hypercapnia on apoptosis when compared with the WT-4HH group (P < 0.05). A2AR deficiency inhibits hippocampal cell apoptosis in mice exposed to chronic hypoxic-hypercapnia, which might be associated with dampened p38 MAPK activation and Bax mRNA expression, and augmented Bcl-2 mRNA expression.

Funder

Key Discipline Construction Foundation of Hwa Mei Hospital, University of Chinese Academy of Sciences, China

Reasearch Foundation of Hwa Mei Hospital, University of Chinese Academy of Sciences, China

Publisher

Oxford University Press (OUP)

Subject

Organic Chemistry,Molecular Biology,Applied Microbiology and Biotechnology,General Medicine,Biochemistry,Analytical Chemistry,Biotechnology

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