N
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.
Journal ArticleDOI
Hemodynamic flow improves rat hepatocyte morphology, function, and metabolic activity in vitro.
Ajit Dash,Michael B. Simmers,Tye G. Deering,Diana J Berry,Ryan E. Feaver,Nicole E. Hastings,Timothy L. Pruett,Edward L. LeCluyse,Brett R. Blackman,Brian R. Wamhoff +9 more
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.
Journal ArticleDOI
PDGF-DD, a novel mediator of smooth muscle cell phenotypic modulation, is upregulated in endothelial cells exposed to atherosclerosis-prone flow patterns
James A. Thomas,Rebecca A. Deaton,Nicole E. Hastings,Yueting Shang,Christopher W. Moehle,Ulf Eriksson,Stavros Topouzis,Brian R. Wamhoff,Brett R. Blackman,Gary K. Owens +9 more
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.