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  • Title: Modulation of the number and functions of endothelial progenitor cells by interleukin 1β in the peripheral blood of pigs: involvement of p38 mitogen-activated protein kinase signaling in vitro.
    Author: Mao A, Liu C, Guo Y, Su D, Luo T, Fu W, Zhou H, Fang G, Sheng Y.
    Journal: J Trauma Acute Care Surg; 2012 Nov; 73(5):1145-51. PubMed ID: 23064606.
    Abstract:
    BACKGROUND: Endothelial progenitor cells (EPCs) have therapeutic potential for the treatment of organ ischemia following trauma or sepsis, frequently associated with inflammatory conditions. We aimed to investigate the effects of interleukin 1β (IL-1β) on the properties of EPCs and explore its possible relationship with p38 mitogen-activated protein kinase (MAPK). METHODS: EPCs were isolated from peripheral blood of a porcine model and were characterized. Effects of IL-1β on cell number, proliferation, migration, adhesion, and angiogenic function of EPCs were evaluated in a time- and dose-dependent manner. The activity of p38 MAPK in EPCs was measured by Western blot. Moreover, the effects of SB203580, a specific p38 MAPK inhibitor, on levels of p38 MAPK phosphorylation and the number and functions of EPCs under IL-1β conditions were examined. RESULTS: Incubation of EPCs with IL-1β (5 ng/mL) for 5 days and with IL-1β (0.05-50 ng/mL) for 48 hours induced a significant reduction in EPC numbers and proliferation, respectively (p < 0.01 vs. control cells). The capacities for migration, adhesion, and angiogenic function of EPCs were also reduced in a time- and dose-dependent manner. IL-1β induced dose- and time-dependent activation of p38 MAPK in EPCs. Moreover, inhibition of p38 MAPK by SB203580 significantly increased the total number of EPCs by twofold as compared with the IL-1β-alone group (p < 0.01) and blocked the ability of IL-1β to impair the functional response of EPCs. CONCLUSION: These results demonstrate that there is a negative cause-effect relationship between IL-1β and EPCs. Thus, IL-1β inhibits EPC proliferation, migration, adhesion, and tube formation by a mechanism, which involves p38 MAPK signaling in regulating the number and functions of EPCs in vitro.
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