Characterization of altered patterns of endothelial progenitor cells in sickle cell disease related pulmonary arterial hypertension
作者： Fatima Anjum , Jason Lazar , Joe Zein , Ghassan Jamaleddine , Spiro Demetis
关键词: Progenitor cell 、 CD34 、 Pathogenesis 、 Pulmonary artery 、 Associated Pulmonary Arterial Hypertension 、 Endothelial dysfunction 、 CD31 、 Vascular resistance 、 Endocrinology 、 Medicine 、 Immunology 、 Internal medicine
摘要: Endothelial dysfunction plays an important role in the pathogenesis of pulmonary arterial hypertension (PAH) sickle cell disease (SCD). A variety evidence suggests that circulating endothelial progenitor cells (EPCs) play integral vascular repair. We hypothesized SCD patients with PAH are deficient EPCs, potentially contributing to and progression. The number CD34+/CD14-/CD106+ EPCs was significantly lower than without (P=0.025). numbers correlated tricuspid regurgitation velocity (TRV, r=-0.44, P=0.033) 6-minute walk distance (6MWD, r= 0.72, P=0.001), mean artery pressure (mPAP, -0.43, P=0.05), resistance (PVR, r=-0.45, P=0.05). Other EPC subsets including CD31+/CD133+/CD146+ were similar between both groups. Numbers did not correlate age, sex, hemoglobin, WBC count, reticulocyte lactate dehydrogenase (LDH), iron/ferritin levels, serum creatinine. These data indicate those PAH. Fewer may contribute pathology. Reduced might only give potential insight into pathophysiological mechanisms but also be useful for identifying suitable therapeutic targets these patients.
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