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Nicole E. Hastings

Researcher at University of Virginia

Publications -  11
Citations -  801

Nicole E. Hastings is an academic researcher from University of Virginia. The author has contributed to research in topics: Endothelial stem cell & Myocyte. The author has an hindex of 9, co-authored 11 publications receiving 747 citations.

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Journal ArticleDOI

Complex regulation and function of the inflammatory smooth muscle cell phenotype in atherosclerosis.

TL;DR: Current knowledge in vascular smooth muscle cell phenotypic modulation is summarized and some of the key unresolved challenges and questions requiring further study are identified.
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Atherosclerosis-prone hemodynamics differentially regulates endothelial and smooth muscle cell phenotypes and promotes pro-inflammatory priming

TL;DR: A novel mechanism whereby modulation of the EC phenotype by hemodynamic shear stresses, atheroprone or atheroprotective, play a critical role in mechanical-transcriptional coupling and regulation of the SMC phenotype is provided.
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Hemodynamic flow improves rat hepatocyte morphology, function, and metabolic activity in vitro.

TL;DR: The retention of in vivo-like hepatocyte phenotype and metabolic function coupled with drug response at more physiological concentrations emphasizes the importance of restoring in vivo physiological transport parameters in vitro.
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GRP78 Upregulation by Atheroprone Shear Stress Via p38-, α2β1-Dependent Mechanism in Endothelial Cells

TL;DR: This study supports a role of the hemodynamic environment in preferentially inducing GRP78 and the UPR in atheroprone regions, before lesion development, and suggests a potential atheroprotective, compensatory effect in response to ER stress within atherosclerotic lesions.
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PDGF-DD, a novel mediator of smooth muscle cell phenotypic modulation, is upregulated in endothelial cells exposed to atherosclerosis-prone flow patterns

TL;DR: It is demonstrated that PDGF-DD inhibited expression of multiple SMC genes, including SM alpha-actin and SM myosin heavy chain, and upregulated expression of the potent SMC differentiation repressor gene Kruppel-like factor-4 at the mRNA and protein levels.