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The Differential Roles of PEA15 Phosphorylations in Reactive Astrogliosis and Astroglial Apoptosis Following Status Epilepticus

The Differential Roles of PEA15 Phosphorylations in Reactive Astrogliosis and Astroglial Apoptosis Following Status Epilepticus

Jin-Young Park, Tae-Cheon Kang

Neurosci Res. 2018 Dec;137:11-22.

PMID: 29438777

Abstract:

Up to this day, the roles of PEA15 expression and its phosphorylation in seizure-related events have not been still unclear. In the present study, we found that PEA15 was distinctly phosphorylated in reactive astrocytes and apoptotic astrocytes in the rat hippocampus following LiCl-pilocarpine-induced status epilepticus (SE, a prolonged seizure activity). PEA15-serine (S) 104 phosphorylation was up-regulated in reactive astrocytes following SE, although PEA15 expression and its S116 phosphorylation were unaltered. Bisindolylmaleimide (BIM), a protein kinase C (PKC) inhibitor, attenuated SE-induced reactive astrogliosis, but phorbol 12-myristate 13-acetate (PMA, a PKC activator) aggravated it. Unlike reactive astrocytes, PEA15-S116 phosphorylation was reduced in apoptotic astrocytes. However, PEA15 expression and its S104 phosphorylation were unchanged in apoptotic astrocyte. Neither BIM nor PMA affected SE-induced astroglial apoptosis. PEA15 expression and its phosphorylations were not relevant to SE-induced CA1 neuronal death. These findings indicate that PEA15-S104 and S116 phosphorylations may play a role in reactive astrogliosis and prevention of astroglial apoptosis, respectively. Therefore, we suggest that the selective manipulation of PEA15 phosphorylations may regulate apoptotic and/or proliferative signals in astrocytes.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP28755035-A	3CAI		28755-03-5	Price

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