Pharmacological stimulation of sigma-1 receptor promotes activation of astrocyte via ERK1/2 and GSK3β signaling pathway

被引:20
作者
Wang, Yun [1 ]
Jiang, Hua-feng [2 ]
Ni, Jing [1 ]
Guo, Lin [1 ,3 ]
机构
[1] Xuzhou Med Univ, Jiangsu Key Lab New Drug Res & Clin Pharm, Xuzhou, Jiangsu, Peoples R China
[2] Huzhou Matern & Child Hlth Care Hosp, Dept Pharm, Huzhou, Zhejiang, Peoples R China
[3] Xuzhou Med Univ, Affiliated Hosp, Dept Pharmacol, Xuzhou, Jiangsu, Peoples R China
基金
中国博士后科学基金; 中国国家自然科学基金;
关键词
Sigma-1; receptor; Astrocyte; Glycogen synthase kinase 3 beta; Extracellular signal-regulated kinases 1/2; REACTIVE GLIOSIS; P38; MAPK; PROLIFERATION; PHOSPHORYLATION; ANTAGONIST; GSK-3-BETA; NEURONS; ROLES; DIFFERENTIATION; INFLAMMATION;
D O I
10.1007/s00210-019-01632-3
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Astrocyte is considered to be a type of passive supportive cells that preserves neuronal activity and survival. The dysfunction of astrocytes is involved in the pathological processes of major depression. Recent studies implicate sigma-1 receptors as putative therapeutic targets for current available antidepressant drugs. However, it is absent of direct evidences whether sigma-1 receptor could promote activation of astrocyte. In the present study, we took advantage of primary astrocyte culture and a highly selective agonist of sigma-1 receptor, (+)SKF-10047 to determine the effect of sigma-1 receptor on Brdu (bromodeoxyuridine) labeling positive cells, migration as well as GFAP (glial fibrillary acidic protein) expression of astrocyte. The results showed that (+)SKF-10047 notably increased the number of Brdu labeling positive cells, migration, and the expression of GFAP in primary astrocytes, which were blocked by antagonist of sigma-1 receptor. Moreover, we also found that (+)SKF-10047 increased the phosphorylation of ERK1/2 (extracellular signal-regulated kinases 1/2) and GSK3 beta (glycogen synthase kinase 3 beta) (ser 9) in the primary astrocytes. In addition, pharmacological inhibition of ERK1/2 and GSK3 beta (ser 9) abolished sigma-1 receptor-promoted activation of astrocyte. Therefore, sigma-1 receptor could be considerate as a new pattern for modulating astrocytic function might emerge as therapeutic strategies.
引用
收藏
页码:801 / 812
页数:12
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