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Jennifer M. Capla

Researcher at New York University

Publications -  12
Citations -  4964

Jennifer M. Capla is an academic researcher from New York University. The author has contributed to research in topics: Progenitor cell & Endothelial stem cell. The author has an hindex of 9, co-authored 12 publications receiving 4753 citations.

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Progenitor cell trafficking is regulated by hypoxic gradients through HIF-1 induction of SDF-1

TL;DR: It is shown that SDF-1 gene expression is regulated by the transcription factor hypoxia-inducible factor-1 (HIF-1) in endothelial cells, resulting in selective in vivo expression of S DF-1 in ischemic tissue in direct proportion to reduced oxygen tension.
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Human Endothelial Progenitor Cells From Type II Diabetics Exhibit Impaired Proliferation, Adhesion, and Incorporation Into Vascular Structures

TL;DR: It is suggested that type II diabetes may alter EPC biology in processes critical for new blood vessel growth and may identify a population at high risk for morbidity and mortality after vascular occlusive events.
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Adult vasculogenesis occurs through in situ recruitment, proliferation, and tubulization of circulating bone marrow-derived cells

TL;DR: It is concluded that BM-derived cells produce new blood vessels via localized recruitment, proliferation, and differentiation of circulating cells in a sequence of events markedly different from existing paradigms of angiogenesis.
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Diabetes impairs endothelial progenitor cell-mediated blood vessel formation in response to hypoxia.

TL;DR: It is suggested that diabetes causes defects in both the endothelial progenitor cell and peripheral tissue responses to hypoxia, and it is unlikely that endothelialprogenitor cell–based cellular therapies will be able to prevent diabetic complications.
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Skin graft vascularization involves precisely regulated regression and replacement of endothelial cells through both angiogenesis and vasculogenesis.

TL;DR: Replacement of the donor graft vasculature by endothelial and endothelial progenitor cells from the recipient along preexisting channels is the predominant mechanism for skin graft revascularization.