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Characterization of altered patterns of endothelial progenitor cells in sickle cell disease related pulmonary arterial hypertension
Endothelial dysfunction plays an important role in the pathogenesis of pulmonary arterial hypertension (PAH) in sickle cell disease (SCD). A variety of evidence suggests that circulating endothelial progenitor cells (EPCs) play an integral role in vascular repair. We hypothesized that SCD patients w...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Medknow Publications & Media Pvt Ltd
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3342749/ https://www.ncbi.nlm.nih.gov/pubmed/22558520 http://dx.doi.org/10.4103/2045-8932.94834 |
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author | Anjum, Fatima Lazar, Jason Zein, Joe Jamaleddine, Ghassan Demetis, Spiro Wadgaonkar, Raj |
author_facet | Anjum, Fatima Lazar, Jason Zein, Joe Jamaleddine, Ghassan Demetis, Spiro Wadgaonkar, Raj |
author_sort | Anjum, Fatima |
collection | PubMed |
description | Endothelial dysfunction plays an important role in the pathogenesis of pulmonary arterial hypertension (PAH) in sickle cell disease (SCD). A variety of evidence suggests that circulating endothelial progenitor cells (EPCs) play an integral role in vascular repair. We hypothesized that SCD patients with PAH are deficient in EPCs, potentially contributing to endothelial dysfunction and disease progression. The number of circulating CD34+/CD14−/CD106+ EPCs was significantly lower in SCD patients with PAH than without PAH (P=0.025). CD34+/CD14−/CD106+ numbers significantly correlated with tricuspid regurgitation velocity (TRV, r=−0.44, P=0.033) 6-minute walk distance (6MWD, r= 0.72, P=0.001), mean pulmonary artery pressure (mPAP, r= −0.43, P=0.05), and pulmonary vascular resistance (PVR, r=−0.45, P=0.05). Other EPC subsets including CD31+/CD133+/CD146+ were similar between both groups. Numbers of EPCs did not correlate with age, sex, hemoglobin, WBC count, reticulocyte count, lactate dehydrogenase (LDH), iron/ferritin levels, and serum creatinine. These data indicate that subsets of EPC are lower in SCD patients with PAH than in those without PAH. Fewer EPCs in PAH patients may contribute to the pulmonary vascular pathology. Reduced number of EPCs in SCD patients with PAH might not only give potential insight into the pathophysiological mechanisms but also might be useful for identifying suitable therapeutic targets in these patients. |
format | Online Article Text |
id | pubmed-3342749 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Medknow Publications & Media Pvt Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-33427492012-05-03 Characterization of altered patterns of endothelial progenitor cells in sickle cell disease related pulmonary arterial hypertension Anjum, Fatima Lazar, Jason Zein, Joe Jamaleddine, Ghassan Demetis, Spiro Wadgaonkar, Raj Pulm Circ Research Article Endothelial dysfunction plays an important role in the pathogenesis of pulmonary arterial hypertension (PAH) in sickle cell disease (SCD). A variety of evidence suggests that circulating endothelial progenitor cells (EPCs) play an integral role in vascular repair. We hypothesized that SCD patients with PAH are deficient in EPCs, potentially contributing to endothelial dysfunction and disease progression. The number of circulating CD34+/CD14−/CD106+ EPCs was significantly lower in SCD patients with PAH than without PAH (P=0.025). CD34+/CD14−/CD106+ numbers significantly correlated with tricuspid regurgitation velocity (TRV, r=−0.44, P=0.033) 6-minute walk distance (6MWD, r= 0.72, P=0.001), mean pulmonary artery pressure (mPAP, r= −0.43, P=0.05), and pulmonary vascular resistance (PVR, r=−0.45, P=0.05). Other EPC subsets including CD31+/CD133+/CD146+ were similar between both groups. Numbers of EPCs did not correlate with age, sex, hemoglobin, WBC count, reticulocyte count, lactate dehydrogenase (LDH), iron/ferritin levels, and serum creatinine. These data indicate that subsets of EPC are lower in SCD patients with PAH than in those without PAH. Fewer EPCs in PAH patients may contribute to the pulmonary vascular pathology. Reduced number of EPCs in SCD patients with PAH might not only give potential insight into the pathophysiological mechanisms but also might be useful for identifying suitable therapeutic targets in these patients. Medknow Publications & Media Pvt Ltd 2012 /pmc/articles/PMC3342749/ /pubmed/22558520 http://dx.doi.org/10.4103/2045-8932.94834 Text en Copyright: © Pulmonary Circulation http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Anjum, Fatima Lazar, Jason Zein, Joe Jamaleddine, Ghassan Demetis, Spiro Wadgaonkar, Raj Characterization of altered patterns of endothelial progenitor cells in sickle cell disease related pulmonary arterial hypertension |
title | Characterization of altered patterns of endothelial progenitor cells in sickle cell disease related pulmonary arterial hypertension |
title_full | Characterization of altered patterns of endothelial progenitor cells in sickle cell disease related pulmonary arterial hypertension |
title_fullStr | Characterization of altered patterns of endothelial progenitor cells in sickle cell disease related pulmonary arterial hypertension |
title_full_unstemmed | Characterization of altered patterns of endothelial progenitor cells in sickle cell disease related pulmonary arterial hypertension |
title_short | Characterization of altered patterns of endothelial progenitor cells in sickle cell disease related pulmonary arterial hypertension |
title_sort | characterization of altered patterns of endothelial progenitor cells in sickle cell disease related pulmonary arterial hypertension |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3342749/ https://www.ncbi.nlm.nih.gov/pubmed/22558520 http://dx.doi.org/10.4103/2045-8932.94834 |
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