T
Theresa R. Krier
Researcher at Indiana University – Purdue University Indianapolis
Publications - 4
Citations - 1743
Theresa R. Krier is an academic researcher from Indiana University – Purdue University Indianapolis. The author has contributed to research in topics: Endothelial stem cell & Neurofibromin 1. The author has an hindex of 4, co-authored 4 publications receiving 1672 citations. Previous affiliations of Theresa R. Krier include Indiana University.
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Journal ArticleDOI
Redefining endothelial progenitor cells via clonal analysis and hematopoietic stem/progenitor cell principals
Mervin C. Yoder,Laura E. Mead,Daniel N. Prater,Theresa R. Krier,Karim N. Mroueh,Fang Li,Rachel Krasich,Constance J. Temm,Josef T. Prchal,David A. Ingram +9 more
TL;DR: It is established that CFU-ECs are not EPCs and the role of these cells in angiogenesis must be re-examined prior to further clinical trials, whereas ECFCs may serve as a potential therapy for vascular regeneration.
Journal ArticleDOI
Clonogenic endothelial progenitor cells are sensitive to oxidative stress.
David A. Ingram,Theresa R. Krier,Laura E. Mead,Colleen McGuire,Daniel N. Prater,Janak R. Bhavsar,M. Reza Saadatzadeh,Khadijeh Bijangi-Vishehsaraei,Fang Li,Mervin C. Yoder,Laura S. Haneline +10 more
TL;DR: A framework for understanding how oxidative injury leads to vascular disease and potentially limits the efficacy of transplantation of EPCs into ischemic tissues enriched for reactive oxygen species and oxidized metabolites is outlined.
Journal ArticleDOI
Neurofibromin is a novel regulator of RAS-induced signals in primary vascular smooth muscle cells
Fang Li,Amy M. Munchhof,Hilary White,Laura E. Mead,Theresa R. Krier,Amy Fenoglio,Shi Chen,Xiaohua Wu,Shanbao Cai,Feng Chun Yang,David A. Ingram +10 more
TL;DR: These studies identify neurofibromin as a novel regulator of Ras activity in VSMCs and provide a framework for understanding cardiovascular disease in NF1 patients and a mechanism by which Ras signals are attenuated for maintaining VSMC homeostasis in blood vessel walls.
Journal ArticleDOI
Neurofibroma-associated growth factors activate a distinct signaling network to alter the function of neurofibromin-deficient endothelial cells
Amy M. Munchhof,Fang Li,Hilary White,Laura E. Mead,Theresa R. Krier,Amy Fenoglio,Xiaohong Li,Jin Yuan,Feng Chun Yang,David A. Ingram +9 more
TL;DR: A discrete Ras effector pathway is identified in Nf1+/- ECs as a potential therapeutic target in the neurofibroma microenvironment, which alters the proliferation and migration of neuro fibromin-deficient ECs in response to neurof fibroma-derived growth factors both in vitro and in vivo.