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Article: Low circulating level of CD133+KDR+cells in patients with systemic sclerosis

TitleLow circulating level of CD133+KDR+cells in patients with systemic sclerosis
Authors
KeywordsDisease activity
Endothelial dysfunction
Endothelial progenitor cells
Systemic sclerosis
Issue Date2010
PublisherPacini Editore SpA. The Journal's web site is located at http://www.clinexprheumatol.org
Citation
Clinical And Experimental Rheumatology, 2010, v. 28 n. 5 SUPPL. 62, p. S19-S25 How to Cite?
AbstractBackground: Results of previous studies on the level of circulating endothelial progenitor cells (EPCs), which are involved in vascular repair, in scleroderma (SSc) patients have been controversial. Objectives: To enumerate circulating EPC subsets and to examine their relation with endothelial dysfunction, biochemical markers of endothelial injury and vascular outcome in SSc patients. Methods: Enumeration of circulating CD34+KDR+ and CD133+ KDR+ EPCs was performed by flow cytometry. Endothelium-dependent vasodilation was evaluated by changes in flow-mediated dilation (FMD%) in the brachial artery. Serum level of vascular endothelial growth factor (VEGF) was measured by enzyme linked immunosorbent assay. Results: SSc patients (n=52) were found to have significantly lower CD133+KDR+EPCs (3.0 vs. 7.0/μl, p<0.001) as well as FMD% (4.8% vs. 7.8%, p<0.001) compared with ageand sex-matched controls (n=52). Among patients who had no concomitant cardiovascular risk factors (n=28), CD133+KDR+ EPC level was significantly lower than controls (3.8 vs. 7.3/μl, p =0.001) and correlated modestly with FMD% (r=0.29, p=0.03). Disease duration was the only determining factor identified for circulating CD133+KDR+ EPCs (p=0.03) by logistic regression analysis. Levels of serum VEGF (p=0.92) and KDR expression were not different between patients who had early and intermediate/late disease. Circulating CD34+KDR+ EPCs was not different between SSc patients and controls and did not correlate with any clinical or biochemical parameter. Conclusion: Lower circulating CDI33 +KDR+ EPC subset was found in SSc patients and correlated with impaired endothelium-dependent vasodilation in patients without cardiovascular risk factors suggesting a potential role of deficient EPC recruitment contributing to endothelial dysfunction in this disease. © Copyright CLINICAL AND.
Persistent Identifierhttp://hdl.handle.net/10722/139481
ISSN
2015 Impact Factor: 2.495
2015 SCImago Journal Rankings: 0.953
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMok, MYen_HK
dc.contributor.authorYiu, KHen_HK
dc.contributor.authorWong, CYen_HK
dc.contributor.authorQiuwaxi, Jen_HK
dc.contributor.authorLai, WHen_HK
dc.contributor.authorWong, WSen_HK
dc.contributor.authorTse, HFen_HK
dc.contributor.authorLau, CSen_HK
dc.date.accessioned2011-09-23T05:50:32Z-
dc.date.available2011-09-23T05:50:32Z-
dc.date.issued2010en_HK
dc.identifier.citationClinical And Experimental Rheumatology, 2010, v. 28 n. 5 SUPPL. 62, p. S19-S25en_HK
dc.identifier.issn0392-856Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/139481-
dc.description.abstractBackground: Results of previous studies on the level of circulating endothelial progenitor cells (EPCs), which are involved in vascular repair, in scleroderma (SSc) patients have been controversial. Objectives: To enumerate circulating EPC subsets and to examine their relation with endothelial dysfunction, biochemical markers of endothelial injury and vascular outcome in SSc patients. Methods: Enumeration of circulating CD34+KDR+ and CD133+ KDR+ EPCs was performed by flow cytometry. Endothelium-dependent vasodilation was evaluated by changes in flow-mediated dilation (FMD%) in the brachial artery. Serum level of vascular endothelial growth factor (VEGF) was measured by enzyme linked immunosorbent assay. Results: SSc patients (n=52) were found to have significantly lower CD133+KDR+EPCs (3.0 vs. 7.0/μl, p<0.001) as well as FMD% (4.8% vs. 7.8%, p<0.001) compared with ageand sex-matched controls (n=52). Among patients who had no concomitant cardiovascular risk factors (n=28), CD133+KDR+ EPC level was significantly lower than controls (3.8 vs. 7.3/μl, p =0.001) and correlated modestly with FMD% (r=0.29, p=0.03). Disease duration was the only determining factor identified for circulating CD133+KDR+ EPCs (p=0.03) by logistic regression analysis. Levels of serum VEGF (p=0.92) and KDR expression were not different between patients who had early and intermediate/late disease. Circulating CD34+KDR+ EPCs was not different between SSc patients and controls and did not correlate with any clinical or biochemical parameter. Conclusion: Lower circulating CDI33 +KDR+ EPC subset was found in SSc patients and correlated with impaired endothelium-dependent vasodilation in patients without cardiovascular risk factors suggesting a potential role of deficient EPC recruitment contributing to endothelial dysfunction in this disease. © Copyright CLINICAL AND.en_HK
dc.languageengen_US
dc.publisherPacini Editore SpA. The Journal's web site is located at http://www.clinexprheumatol.orgen_HK
dc.relation.ispartofClinical and Experimental Rheumatologyen_HK
dc.subjectDisease activityen_HK
dc.subjectEndothelial dysfunctionen_HK
dc.subjectEndothelial progenitor cellsen_HK
dc.subjectSystemic sclerosisen_HK
dc.subject.meshAntigens, CD - metabolism-
dc.subject.meshEndothelium, Vascular - metabolism - pathology-
dc.subject.meshGlycoproteins - metabolism-
dc.subject.meshPeptides - metabolism-
dc.subject.meshStem Cells - metabolism - pathology-
dc.titleLow circulating level of CD133+KDR+cells in patients with systemic sclerosisen_HK
dc.typeArticleen_HK
dc.identifier.emailMok, MY:temy@hkucc.hku.hken_HK
dc.identifier.emailYiu, KH:khkyiu@hku.hken_HK
dc.identifier.emailTse, HF:hftse@hkucc.hku.hken_HK
dc.identifier.emailLau, CS:cslau@hku.hken_HK
dc.identifier.authorityMok, MY=rp00490en_HK
dc.identifier.authorityYiu, KH=rp01490en_HK
dc.identifier.authorityTse, HF=rp00428en_HK
dc.identifier.authorityLau, CS=rp01348en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid21050541-
dc.identifier.scopuseid_2-s2.0-78650557653en_HK
dc.identifier.hkuros195382en_US
dc.identifier.hkuros174743-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78650557653&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume28en_HK
dc.identifier.issue5 SUPPL. 62en_HK
dc.identifier.spageS19en_HK
dc.identifier.epageS25en_HK
dc.identifier.isiWOS:000284028600005-
dc.publisher.placeItalyen_HK
dc.identifier.scopusauthoridMok, MY=7006024184en_HK
dc.identifier.scopusauthoridYiu, KH=35172267800en_HK
dc.identifier.scopusauthoridWong, CY=14824318400en_HK
dc.identifier.scopusauthoridQiuwaxi, J=25923529900en_HK
dc.identifier.scopusauthoridLai, WH=36790434600en_HK
dc.identifier.scopusauthoridWong, WS=8737892100en_HK
dc.identifier.scopusauthoridTse, HF=7006070805en_HK
dc.identifier.scopusauthoridLau, CS=14035682100en_HK

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