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The Adipokines Leptin and Resistin Modulate Endothelial Progenitor Cells
Author(s) -
Zhang Yanhua,
Zhang Yanmin,
Mead Laura E,
Prater Daniel,
Ingram David A,
Rehman Jalees
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a379-e
Subject(s) - adipokine , resistin , leptin , progenitor cell , medicine , endocrinology , angiogenesis , adipose tissue , endothelial stem cell , endothelial progenitor cell , paracrine signalling , stem cell , biology , microbiology and biotechnology , obesity , biochemistry , receptor , in vitro
Endothelial Progenitor Cells (EPCs) are circulating cells which appear to play a major role in endothelial repair and angiogenesis. Obesity contributes to endothelial dysfunction in part by the adipose tissue releasing harmful paracrine factors (adipokines) like leptin and resistin. We studied whether such adipokines were also able to affect EPCs. Methods: Colony‐forming Endothelial Progenitor Cells (EPCs) were isolated from umbilical cord blood as previously published. For the adipokine growth assay, EPCs were plated in 96‐well plates and exposed to either leptin or resistin (dose ranges 0.1 ng/ml to 100 ng/ml) for 48 hours. At the end of the treatment period, cell growth was measured with the MTT assay using published methods. Data is presented as mean absorbance at 570 nm of multiple experiments. Results: Exposure to leptin and resistin was able to modulate the growth of EPCs in the physiologic and pathophysiologic dose range. For example, leptin reduced EPC growth from 0.51±0.03 at the physiologic plasma levels of 10 ng/ml to 0.40±0.08 when EPCs were exposed to leptin levels of 100 ng/ml, which are found in obesity. Conclusions: While previous studies have demonstrated adipokine effects on endothelial cells, our data suggests that adipokines are also able to act on endothelial progenitor cells. Since EPCs are critical for maintaining vascular health, detrimental effects of adipokines on EPCs may contribute to the development of cardiovascular disease. Further studies are needed to compare the vulnerability of EPCs and mature endothelial cells in patients with obesity.