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Article: Low circulating level of CD133+KDR+cells in patients with systemic sclerosis
Title | Low circulating level of CD133+KDR+cells in patients with systemic sclerosis |
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Authors | |
Keywords | Disease activity Endothelial dysfunction Endothelial progenitor cells Systemic sclerosis |
Issue Date | 2010 |
Publisher | Pacini 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? |
Abstract | Background: 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 Identifier | http://hdl.handle.net/10722/139481 |
ISSN | 2023 Impact Factor: 3.4 2023 SCImago Journal Rankings: 0.907 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Mok, MY | en_HK |
dc.contributor.author | Yiu, KH | en_HK |
dc.contributor.author | Wong, CY | en_HK |
dc.contributor.author | Qiuwaxi, J | en_HK |
dc.contributor.author | Lai, WH | en_HK |
dc.contributor.author | Wong, WS | en_HK |
dc.contributor.author | Tse, HF | en_HK |
dc.contributor.author | Lau, CS | en_HK |
dc.date.accessioned | 2011-09-23T05:50:32Z | - |
dc.date.available | 2011-09-23T05:50:32Z | - |
dc.date.issued | 2010 | en_HK |
dc.identifier.citation | Clinical And Experimental Rheumatology, 2010, v. 28 n. 5 SUPPL. 62, p. S19-S25 | en_HK |
dc.identifier.issn | 0392-856X | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/139481 | - |
dc.description.abstract | Background: 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.language | eng | en_US |
dc.publisher | Pacini Editore SpA. The Journal's web site is located at http://www.clinexprheumatol.org | en_HK |
dc.relation.ispartof | Clinical and Experimental Rheumatology | en_HK |
dc.subject | Disease activity | en_HK |
dc.subject | Endothelial dysfunction | en_HK |
dc.subject | Endothelial progenitor cells | en_HK |
dc.subject | Systemic sclerosis | en_HK |
dc.subject.mesh | Antigens, CD - metabolism | - |
dc.subject.mesh | Endothelium, Vascular - metabolism - pathology | - |
dc.subject.mesh | Glycoproteins - metabolism | - |
dc.subject.mesh | Peptides - metabolism | - |
dc.subject.mesh | Stem Cells - metabolism - pathology | - |
dc.title | Low circulating level of CD133+KDR+cells in patients with systemic sclerosis | en_HK |
dc.type | Article | en_HK |
dc.identifier.email | Mok, MY:temy@hkucc.hku.hk | en_HK |
dc.identifier.email | Yiu, KH:khkyiu@hku.hk | en_HK |
dc.identifier.email | Tse, HF:hftse@hkucc.hku.hk | en_HK |
dc.identifier.email | Lau, CS:cslau@hku.hk | en_HK |
dc.identifier.authority | Mok, MY=rp00490 | en_HK |
dc.identifier.authority | Yiu, KH=rp01490 | en_HK |
dc.identifier.authority | Tse, HF=rp00428 | en_HK |
dc.identifier.authority | Lau, CS=rp01348 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.pmid | 21050541 | - |
dc.identifier.scopus | eid_2-s2.0-78650557653 | en_HK |
dc.identifier.hkuros | 195382 | en_US |
dc.identifier.hkuros | 174743 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-78650557653&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 28 | en_HK |
dc.identifier.issue | 5 SUPPL. 62 | en_HK |
dc.identifier.spage | S19 | en_HK |
dc.identifier.epage | S25 | en_HK |
dc.identifier.isi | WOS:000284028600005 | - |
dc.publisher.place | Italy | en_HK |
dc.identifier.scopusauthorid | Mok, MY=7006024184 | en_HK |
dc.identifier.scopusauthorid | Yiu, KH=35172267800 | en_HK |
dc.identifier.scopusauthorid | Wong, CY=14824318400 | en_HK |
dc.identifier.scopusauthorid | Qiuwaxi, J=25923529900 | en_HK |
dc.identifier.scopusauthorid | Lai, WH=36790434600 | en_HK |
dc.identifier.scopusauthorid | Wong, WS=8737892100 | en_HK |
dc.identifier.scopusauthorid | Tse, HF=7006070805 | en_HK |
dc.identifier.scopusauthorid | Lau, CS=14035682100 | en_HK |
dc.identifier.issnl | 0392-856X | - |