Phosphorylation of cAMP-Activated Exchange Protein-1 Participates in Neuroprotection and Ferroptosis Regulation Following Intracerebral Hemorrhage in Rats.

ABSTRACT:

Background

Intracerebral hemorrhage (ICH) is a severe condition characterized by elevated mortality and disability rates. The cAMP-activated exchange protein-1 (EPAC-1) is implicated in various cytoprotective mechanisms; however, its specific role in ICH remains unclear.

Methods

A rat model of ICH was established by injecting autologous blood, while the in vitro primary neuronal model was stimulated using oxyhemoglobin (OxyHb). The construction of EPAC-1 overexpression wild-type (WT) and phosphorylated mutant plasmids (S108A or S108E), as well as lentiviruses, was performed for in vitro and in vivo studies.

Results

The cAMP signaling pathway was found to be significantly enriched following ICH by high-throughput sequencing analysis. Our findings showed that while EPAC

SUBMITTER: Jiang G 

PROVIDER: S-EPMC11979711 | biostudies-literature | 2025 Apr

REPOSITORIES: biostudies-literature