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Stem cells mobilization and vasculogenesis in vivo stimulated by lactic acid and hyperbaric oxygen
Author(s) -
Milovanova Tatya.,
Moore Jonni S.,
Hunt Thomas K.,
Thom Stephen R.
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.a381-a
Subject(s) - vasculogenesis , matrigel , progenitor cell , in vivo , bone marrow , chemistry , angiogenesis , endothelial progenitor cell , stem cell , andrology , immunology , medicine , microbiology and biotechnology , biology
Lactic acid is a constant feature of ischemic wounds and exposure to hyperbaric oxygen (HBO 2 ) has been shown to mobilize stem/progenitor cells (SPCs) from bone marrow to peripheral circulation. We hypothesized that lactic acid and/or HBO 2 exposure contribute to neovascularization by differentiation or/and proliferation of SPCs in vivo . Matrigel implants with or without lactate were placed subcutaneously in mice, some were left to breathe room air (control) and some were exposed daily for 1.5 h to HBO 2 at a pressure of 2.8 atmosphere absolute (ATA). Using multiparameter flow cytometry, we analyzed various progenitor subsets defined by the expression of CD34 and/or CD133, CD 31, Sca‐1, VEGFR2 and CXCR4 markers and quantified the absolute numbers of SPCs in both types of matrigel, blood and bone marrow at 5 and 10 days. Collected cells were also assessed for cell cycle and percent apoptosis. HBO 2 mobilized SPCs determined by a 3–5 fold elevation in peripheral blood. In air‐breathing control mice, matrigel + lactate exhibited 2 fold greater SPCs versus non‐supplemented Matrigel, and the combination of HBO 2 and lactate resulted in a 3–6 fold elevation in SPCs number as well as enhancement of cell cycle progression (S+G 2 /M phase elevation). This is the first report demonstrating that lactate can stimulate SPCs recruitment and differentiation. This 3‐D model will be useful to study the physiology of vasculogenesis and methods to accelerate wound healing [AT00428].