Endothelial microparticles and progenitor cells in pulmonary arterial hypertension

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Rationale and aim: Endothelial dysfunction is crucial for the development of pulmonary arterial hypertension (PAH). The combined assessment of endothelial microparticles (EMPs) and progenitor cells (PCs) informs about endothelial impairment and endogenous repair capacity. Accordingly, we aimed to assess the number of circulating EMPs and PCs in PAH patients and investigate whether indices of PAH severity correlate with these cytometric measurements. Methods: Circulating EMPs and PCs were determined in 53 controls (51±12y; 78% females) and 71 PAH patients (53±16y; 77% females; mPAP 46±12 mmHg) all of them under specific theraphy. Total (CD31+CD42b-), apoptotic (CD31+CD42b-AnnexinV+) and activated (CD31+CD42b-CD62E+) EMPs were determined by flow cytometry in platelet poor plasma. Circulating PCs (CD34+CD45+, CD34+CD133+ and c-Kit+ cells) were measured from mononuclear peripheral blood cells by flow cytometry. Results: Total circulating EMPs were increased in PAH (median, 600 (IQR, 358-871) EMPs/μl) compared with controls (428 (299-633) EMPs/μl) (p<0.05). Apoptotic EMPs were also higher in PAH compared with controls (353 (212-588) vs 261 (195-367) EMPs/μl; p<0.05). No differences were observed in activated EMPs. The number of the three assessed circulating PCs were reduced in PAH compared with controls (p<0.05). No correlation was found between circulating EMPs and PCs numbers and with PAH severity. Conclusions: Patients with PAH show endothelial impairment and reduced repair capacity, as shown by increased circulating EMPs and reduced PCs. Supported by FIS PS12/00510. J. Garcia-Lucio is recipient of PFIS grant from ISCIII.

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