Subarachnoid hemorrhage-associated brain injury and neurobehavioral deficits are reversed with synthetic adropin treatment through sustained Ser1179 phosphorylation of endothelial nitric oxide synthase.

ABSTRACT:

Background

Subarachnoid hemorrhage (SAH) is a life-threatening vascular condition without satisfactory treatment options. The secreted peptide adropin is highly expressed in the human brain and has neuroprotective effects in brain injury models, including actions involving the cerebrovasculature. Here, we report an endothelial nitric oxide synthase (eNOS)-dependent effect of synthetic adropin treatment that reverses the deleterious effects of SAH.

Methods

We tested the molecular, cellular, and physiological responses of cultured brain microvascular endothelial cells and two mouse models of SAH to treatment using synthetic adropin peptide or vehicle.

Results

SAH decreases adropin expression in cultured brain microvascular endothelial cells and in murine brain tissue. I

SUBMITTER: Dodd WS 

PROVIDER: S-EPMC11434178 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature