Endothelial Dysfunction in Human Diabetes Is Mediated by Wnt5a-JNK Signaling.

ABSTRACT:

Objective

Endothelial dysfunction is linked to insulin resistance, inflammatory activation, and increased cardiovascular risk in diabetes mellitus; however, the mechanisms remain incompletely understood. Recent studies have identified proinflammatory signaling of wingless-type family member (Wnt) 5a through c-jun N-terminal kinase (JNK) as a regulator of metabolic dysfunction with potential relevance to vascular function. We sought to gain evidence that increased activation of Wnt5a-JNK signaling contributes to impaired endothelial function in patients with diabetes mellitus.

Approach and results

We measured flow-mediated dilation of the brachial artery and characterized freshly isolated endothelial cells by protein expression, eNOS activation, and nitric oxide production in

SUBMITTER: Breton-Romero R 

PROVIDER: S-EPMC4913891 | biostudies-literature | 2016 Mar

REPOSITORIES: biostudies-literature