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Mobilization of angiogenic monocytes in response to induced remote ischemia in healthy subjects
Author(s) -
Resende Micheline M,
Gahremanpour Amir,
CabreiraHansen Maria Graca,
Wang Xiaohong,
Willerson James T,
Silva Guilherme,
Perin Emerson
Publication year - 2013
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.27.1_supplement.lb685
Subject(s) - ischemia , medicine , progenitor cell , cd14 , flow cytometry , immunology , stem cell , biology , microbiology and biotechnology
Mobilization of circulating progenitor cells (CPC) or discrete hematopoietic cell subsets (HCS) has been studied in a variety of scenarios. Variability in ischemia duration and lack of appropriate controls are challenges in interpreting the often‐conflicting results of these studies. We studied the ischemia‐induced changes in CPC and HCS in healthy adults (age 18–25). Changes in PC and HCS levels were compared between normal physiological (N=4) conditions and induced transient ischemia (N=8) by flow cytometry and colony‐forming assay (CFU‐Hill). Ischemia was induced by 5 cycles of ischemia‐reperfusion using a pressure cuff around the thigh. Number of CFU‐HIL, levels of CPC, HCS were analyzed at baseline, 6, 24, 48, 72 hours and 7days post‐ischemia. In contrast to the controls, there was a rise in angiogenic monocytes, Tie‐2+ CD14+ CD16mid cells (ANM) at 48h (0.19 ± 0.09 vs 0.40 ± 0.007% p<0.05) compared to baseline, while other populations remained unchanged. ANM have an important role in the maintenance of the endothelial integrity after ischemia by recruiting endothelial cells. In conclusion, our study is the first to show that ANM are mobilized in response to tissue ischemia in healthy subjects. This may reflect normal function of the vascular endothelium in response to ischemia, and suggests that this non‐invasive maneuver may be used as a potential new approach to access the role of ANM in vascular biology.