scispace - formally typeset
W

Wanda S. LeJeune

Researcher at University of Texas Medical Branch

Publications -  19
Citations -  1497

Wanda S. LeJeune is an academic researcher from University of Texas Medical Branch. The author has contributed to research in topics: Proinflammatory cytokine & Hemodynamics. The author has an hindex of 16, co-authored 19 publications receiving 1360 citations. Previous affiliations of Wanda S. LeJeune include Washington University in St. Louis.

Papers
More filters
Journal ArticleDOI

An adventitial IL-6/MCP1 amplification loop accelerates macrophage-mediated vascular inflammation leading to aortic dissection in mice

TL;DR: Results suggest that leukocyte-fibroblast interactions in the aortic adventitia potentiate IL-6 production, inducing local monocyte recruitment and activation, thereby promoting MCP-1 secretion, vascular inflammation, ECM remodeling, and aortIC destabilization.
Journal ArticleDOI

Klotho depletion contributes to increased inflammation in kidney of the db/db mouse model of diabetes via RelA (serine)536 phosphorylation.

TL;DR: Findings suggest that Klotho serves as an anti-inflammatory modulator, negatively regulating the production of NF-κB–linked inflammatory proteins via a mechanism that involves phosphorylation of Ser536 in the transactivation domain of RelA.
Journal Article

Role for nitric oxide in the hyperpermeability and hemodynamic changes induced by intravenous VEGF.

TL;DR: Intravenous infusion of VEGF can acutely impair endothelial cell barrier functional integrity and relax resistance arterioles in ocular tissues and brain through a mechanism involving activation of NOS.
Journal ArticleDOI

Angiotensin II induces IL-6 expression and the Jak-STAT3 pathway in aortic adventitia of LDL receptor-deficient mice

TL;DR: It is demonstrated that IL-6, produced by activated macrophages and fibroblasts in the adventitia, induces the Jak-STAT3 pathway during early A-II-induced atherosclerosis.
Journal ArticleDOI

Interleukin-6–Signal Transducer and Activator of Transcription-3 Signaling Mediates Aortic Dissections Induced by Angiotensin II via the T-Helper Lymphocyte 17–Interleukin 17 Axis in C57BL/6 Mice

TL;DR: The results indicate that the IL-6–signal transducer and activator of transcription-3 signaling pathway converges on Th17 recruitment and IL-17A signaling upstream of macrophage recruitment, mediating aortic dissections.