Protein kinase B (AKT) upregulation and Thy-1-α_vβ₃ integrin-induced phosphorylation of Connexin43 by activated AKT in astrogliosis.

ABSTRACT:

Background

In response to brain injury or inflammation, astrocytes undergo hypertrophy, proliferate, and migrate to the damaged zone. These changes, collectively known as "astrogliosis", initially protect the brain; however, astrogliosis can also cause neuronal dysfunction. Additionally, these astrocytes undergo intracellular changes involving alterations in the expression and localization of many proteins, including α_vβ₃ integrin. Our previous reports indicate that Thy-1, a neuronal glycoprotein, binds to this integrin inducing Connexin43 (Cx43) hemichannel (HC) opening, ATP release, and astrocyte migration. Despite such insight, important links and molecular events leading to astrogliosis remain to be defined.

Methods

Using bioinformatics approaches,

SUBMITTER: Perez-Nunez R 

PROVIDER: S-EPMC9817390 | biostudies-literature | 2023 Jan

REPOSITORIES: biostudies-literature