Obesity impairs wound closure through a vasculogenic mechanism.

摘要: Since obesity impairs wound healing and bone marrow (BM)-derived vasculogenic progenitor cells (PCs) are important for tissue repair, we hypothesize that obesity-impaired is due, in part, to impaired PC mobilization, trafficking, function. Peripheral blood was obtained from nondiabetic, obese (BMI > 30, n = 25), nonobese < 17) subjects. human (h)PCs were isolated, quantified, functionally assessed. To corroborate the experiments, 6-mm stented wounds created on nondiabetic mice (TALLYHO/JngJ, 15) (SWR/J, 15). mouse (m)PCs quantified analyzed. There no difference number of baseline circulating hPCs (hPC-ob), (hPC-nl) subjects, but hPC-ob had adhesion (p 0.05), migration 0.01), proliferation 0.001). Nondiabetic a significant decrease PCs (mPC-ob) at 7 0.008) 14 days 0.003) after wounding. The mPC-ob response correlated with significantly closure 0.001) 21 as well fewer new vessels Our results suggest BM-derived peripheral injury this, turn, closure.