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Diabetes mellitus impairs CD133+ progenitor cell function after myocardial infarction
. Background. Circulating progenitor cells (PC) can positively influence the healing of ischaemic myocardium. Cardiovascular risk factors including diabetes mellitus (DM) may have a negative influence on both number and recruitment of PC. Recent evidence suggests that less differentiated CD133+PC c...
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| Published in: | Journal of internal medicine 2009-02, Vol.265 (2), p.238-249 |
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| container_title | Journal of internal medicine |
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| creator | Vöö, S. Dunaeva, M. Eggermann, J. Stadler, N. Waltenberger, J. |
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Background. Circulating progenitor cells (PC) can positively influence the healing of ischaemic myocardium. Cardiovascular risk factors including diabetes mellitus (DM) may have a negative influence on both number and recruitment of PC. Recent evidence suggests that less differentiated CD133+PC contribute to myocardial healing and are promising candidates for therapy. Therefore, we investigated whether DM affects CD133+PC.
Methods. CD133+PC were analyzed in patients following acute myocardial infarction and successful reperfusion [acute myocardial infarction (AMI, n = 45) with/without non‐insulin‐requiring type 2 DM (T2DM)]. Stable coronary artery disease patients (CAD, n = 45) served as stable controls. Number and phenotype of CD133+PC were assessed by flow cytometry. CD133+PC chemotaxis was assessed towards vascular endothelial growth factor, an angiogenic stimulus upregulated in AMI. The expression of anti‐oxidant enzymes in CD133+PC was detected by reverse‐transcriptase PCR.
Results. In non‐DM patients, the number of CD133+PC increased on day 3 following AMI (P = 0.0001). In contrast, no changes were observed in AMI patients with T2DM. Regarding the function of CD133+PC, an enhanced chemotactic response was observed following AMI in both non‐DM (P = 0.0001) and T2DM (P = 0.007). However, the AMI‐related functional activation was significantly weaker in diabetic patients (P = 0.001). Moreover, the expression of catalase was lower in CD133+PC from T2DM.
Conclusions. Our results show that T2DM not only limits the abundance of CD133+PC following AMI, but also limits their activation. This might be explained by a lower resistance of CD133+PC to oxidative stress. Our data provide a possible explanation for the delayed postischaemic vascular healing and myocardial recovery in DM. |
| doi_str_mv | 10.1111/j.1365-2796.2008.02011.x |
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| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_66886833</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>66886833</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4481-4202d3c818f2b46456a4991c6d7cd8f94e80d41c58382ac953f83b6731cfb27d3</originalsourceid><addsrcrecordid>eNqNkE1P3DAQhq2KqmyBv4B8gUuVdMZ2vPalUrX0g4qKSzlbjmMjr_Kx2Ilg_30TdkWv9WUszTMzrx5CKEKJ8_u8LZHLqmBrLUsGoEpggFi-vCOrt8YJWYGuRCEVg1PyMectAHKQ8IGcogbUqMWKPNxEW_vRZ9r5to3jlGnsdjamTDc3yPknukvDo-_jOCTqZoSGqXdjHHpqw-gT7faDs6mJtqWxDza99s7J-2Db7C-O9Yw8fP_2Z_OzuLv_cbv5elc4IRQWggFruFOoAquFFJW0Qmt0slm7RgUtvIJGoKsUV8w6XfGgeC3XHF2o2brhZ-T6sHcO-TT5PJou5iWl7f0wZSOlUlJxPoPqALo05Jx8MLsUO5v2BsEsSs3WLObMYs4sSs2rUvMyj14eb0x155t_g0eHM3B1BGx2tg3J9i7mN44hcKhkNXNfDtxzbP3-vwOYX_e3v5cv_wtMK5Fb</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>66886833</pqid></control><display><type>article</type><title>Diabetes mellitus impairs CD133+ progenitor cell function after myocardial infarction</title><source>Wiley-Blackwell Read & Publish Collection</source><creator>Vöö, S. ; Dunaeva, M. ; Eggermann, J. ; Stadler, N. ; Waltenberger, J.</creator><creatorcontrib>Vöö, S. ; Dunaeva, M. ; Eggermann, J. ; Stadler, N. ; Waltenberger, J.</creatorcontrib><description>.
Background. Circulating progenitor cells (PC) can positively influence the healing of ischaemic myocardium. Cardiovascular risk factors including diabetes mellitus (DM) may have a negative influence on both number and recruitment of PC. Recent evidence suggests that less differentiated CD133+PC contribute to myocardial healing and are promising candidates for therapy. Therefore, we investigated whether DM affects CD133+PC.
Methods. CD133+PC were analyzed in patients following acute myocardial infarction and successful reperfusion [acute myocardial infarction (AMI, n = 45) with/without non‐insulin‐requiring type 2 DM (T2DM)]. Stable coronary artery disease patients (CAD, n = 45) served as stable controls. Number and phenotype of CD133+PC were assessed by flow cytometry. CD133+PC chemotaxis was assessed towards vascular endothelial growth factor, an angiogenic stimulus upregulated in AMI. The expression of anti‐oxidant enzymes in CD133+PC was detected by reverse‐transcriptase PCR.
Results. In non‐DM patients, the number of CD133+PC increased on day 3 following AMI (P = 0.0001). In contrast, no changes were observed in AMI patients with T2DM. Regarding the function of CD133+PC, an enhanced chemotactic response was observed following AMI in both non‐DM (P = 0.0001) and T2DM (P = 0.007). However, the AMI‐related functional activation was significantly weaker in diabetic patients (P = 0.001). Moreover, the expression of catalase was lower in CD133+PC from T2DM.
Conclusions. Our results show that T2DM not only limits the abundance of CD133+PC following AMI, but also limits their activation. This might be explained by a lower resistance of CD133+PC to oxidative stress. Our data provide a possible explanation for the delayed postischaemic vascular healing and myocardial recovery in DM.</description><identifier>ISSN: 0954-6820</identifier><identifier>EISSN: 1365-2796</identifier><identifier>DOI: 10.1111/j.1365-2796.2008.02011.x</identifier><identifier>PMID: 19019194</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>AC133 Antigen ; acute myocardial infarction ; Aged ; Antigens, CD ; Biological and medical sciences ; Biomarkers ; CD133 ; Chemotaxis - physiology ; coronary heart disease ; diabetes mellitus ; Diabetes Mellitus, Type 2 - blood ; Diabetes. Impaired glucose tolerance ; Diabetic Angiopathies - blood ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Female ; Flow Cytometry ; General aspects ; Glycoproteins ; Humans ; Male ; Medical sciences ; Middle Aged ; Myocardial Infarction - blood ; Myocardial Infarction - pathology ; Peptides ; Pilot Projects ; progenitor cells ; Prospective Studies ; Stem Cells - physiology ; Vascular Endothelial Growth Factor Receptor-1 - blood</subject><ispartof>Journal of internal medicine, 2009-02, Vol.265 (2), p.238-249</ispartof><rights>2008 Blackwell Publishing Ltd</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4481-4202d3c818f2b46456a4991c6d7cd8f94e80d41c58382ac953f83b6731cfb27d3</citedby><cites>FETCH-LOGICAL-c4481-4202d3c818f2b46456a4991c6d7cd8f94e80d41c58382ac953f83b6731cfb27d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21030565$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19019194$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vöö, S.</creatorcontrib><creatorcontrib>Dunaeva, M.</creatorcontrib><creatorcontrib>Eggermann, J.</creatorcontrib><creatorcontrib>Stadler, N.</creatorcontrib><creatorcontrib>Waltenberger, J.</creatorcontrib><title>Diabetes mellitus impairs CD133+ progenitor cell function after myocardial infarction</title><title>Journal of internal medicine</title><addtitle>J Intern Med</addtitle><description>.
Background. Circulating progenitor cells (PC) can positively influence the healing of ischaemic myocardium. Cardiovascular risk factors including diabetes mellitus (DM) may have a negative influence on both number and recruitment of PC. Recent evidence suggests that less differentiated CD133+PC contribute to myocardial healing and are promising candidates for therapy. Therefore, we investigated whether DM affects CD133+PC.
Methods. CD133+PC were analyzed in patients following acute myocardial infarction and successful reperfusion [acute myocardial infarction (AMI, n = 45) with/without non‐insulin‐requiring type 2 DM (T2DM)]. Stable coronary artery disease patients (CAD, n = 45) served as stable controls. Number and phenotype of CD133+PC were assessed by flow cytometry. CD133+PC chemotaxis was assessed towards vascular endothelial growth factor, an angiogenic stimulus upregulated in AMI. The expression of anti‐oxidant enzymes in CD133+PC was detected by reverse‐transcriptase PCR.
Results. In non‐DM patients, the number of CD133+PC increased on day 3 following AMI (P = 0.0001). In contrast, no changes were observed in AMI patients with T2DM. Regarding the function of CD133+PC, an enhanced chemotactic response was observed following AMI in both non‐DM (P = 0.0001) and T2DM (P = 0.007). However, the AMI‐related functional activation was significantly weaker in diabetic patients (P = 0.001). Moreover, the expression of catalase was lower in CD133+PC from T2DM.
Conclusions. Our results show that T2DM not only limits the abundance of CD133+PC following AMI, but also limits their activation. This might be explained by a lower resistance of CD133+PC to oxidative stress. Our data provide a possible explanation for the delayed postischaemic vascular healing and myocardial recovery in DM.</description><subject>AC133 Antigen</subject><subject>acute myocardial infarction</subject><subject>Aged</subject><subject>Antigens, CD</subject><subject>Biological and medical sciences</subject><subject>Biomarkers</subject><subject>CD133</subject><subject>Chemotaxis - physiology</subject><subject>coronary heart disease</subject><subject>diabetes mellitus</subject><subject>Diabetes Mellitus, Type 2 - blood</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Diabetic Angiopathies - blood</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>General aspects</subject><subject>Glycoproteins</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Myocardial Infarction - blood</subject><subject>Myocardial Infarction - pathology</subject><subject>Peptides</subject><subject>Pilot Projects</subject><subject>progenitor cells</subject><subject>Prospective Studies</subject><subject>Stem Cells - physiology</subject><subject>Vascular Endothelial Growth Factor Receptor-1 - blood</subject><issn>0954-6820</issn><issn>1365-2796</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><recordid>eNqNkE1P3DAQhq2KqmyBv4B8gUuVdMZ2vPalUrX0g4qKSzlbjmMjr_Kx2Ilg_30TdkWv9WUszTMzrx5CKEKJ8_u8LZHLqmBrLUsGoEpggFi-vCOrt8YJWYGuRCEVg1PyMectAHKQ8IGcogbUqMWKPNxEW_vRZ9r5to3jlGnsdjamTDc3yPknukvDo-_jOCTqZoSGqXdjHHpqw-gT7faDs6mJtqWxDza99s7J-2Db7C-O9Yw8fP_2Z_OzuLv_cbv5elc4IRQWggFruFOoAquFFJW0Qmt0slm7RgUtvIJGoKsUV8w6XfGgeC3XHF2o2brhZ-T6sHcO-TT5PJou5iWl7f0wZSOlUlJxPoPqALo05Jx8MLsUO5v2BsEsSs3WLObMYs4sSs2rUvMyj14eb0x155t_g0eHM3B1BGx2tg3J9i7mN44hcKhkNXNfDtxzbP3-vwOYX_e3v5cv_wtMK5Fb</recordid><startdate>200902</startdate><enddate>200902</enddate><creator>Vöö, S.</creator><creator>Dunaeva, M.</creator><creator>Eggermann, J.</creator><creator>Stadler, N.</creator><creator>Waltenberger, J.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>200902</creationdate><title>Diabetes mellitus impairs CD133+ progenitor cell function after myocardial infarction</title><author>Vöö, S. ; Dunaeva, M. ; Eggermann, J. ; Stadler, N. ; Waltenberger, J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4481-4202d3c818f2b46456a4991c6d7cd8f94e80d41c58382ac953f83b6731cfb27d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>AC133 Antigen</topic><topic>acute myocardial infarction</topic><topic>Aged</topic><topic>Antigens, CD</topic><topic>Biological and medical sciences</topic><topic>Biomarkers</topic><topic>CD133</topic><topic>Chemotaxis - physiology</topic><topic>coronary heart disease</topic><topic>diabetes mellitus</topic><topic>Diabetes Mellitus, Type 2 - blood</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Diabetic Angiopathies - blood</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Female</topic><topic>Flow Cytometry</topic><topic>General aspects</topic><topic>Glycoproteins</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Myocardial Infarction - blood</topic><topic>Myocardial Infarction - pathology</topic><topic>Peptides</topic><topic>Pilot Projects</topic><topic>progenitor cells</topic><topic>Prospective Studies</topic><topic>Stem Cells - physiology</topic><topic>Vascular Endothelial Growth Factor Receptor-1 - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vöö, S.</creatorcontrib><creatorcontrib>Dunaeva, M.</creatorcontrib><creatorcontrib>Eggermann, J.</creatorcontrib><creatorcontrib>Stadler, N.</creatorcontrib><creatorcontrib>Waltenberger, J.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of internal medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vöö, S.</au><au>Dunaeva, M.</au><au>Eggermann, J.</au><au>Stadler, N.</au><au>Waltenberger, J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Diabetes mellitus impairs CD133+ progenitor cell function after myocardial infarction</atitle><jtitle>Journal of internal medicine</jtitle><addtitle>J Intern Med</addtitle><date>2009-02</date><risdate>2009</risdate><volume>265</volume><issue>2</issue><spage>238</spage><epage>249</epage><pages>238-249</pages><issn>0954-6820</issn><eissn>1365-2796</eissn><abstract>.
Background. Circulating progenitor cells (PC) can positively influence the healing of ischaemic myocardium. Cardiovascular risk factors including diabetes mellitus (DM) may have a negative influence on both number and recruitment of PC. Recent evidence suggests that less differentiated CD133+PC contribute to myocardial healing and are promising candidates for therapy. Therefore, we investigated whether DM affects CD133+PC.
Methods. CD133+PC were analyzed in patients following acute myocardial infarction and successful reperfusion [acute myocardial infarction (AMI, n = 45) with/without non‐insulin‐requiring type 2 DM (T2DM)]. Stable coronary artery disease patients (CAD, n = 45) served as stable controls. Number and phenotype of CD133+PC were assessed by flow cytometry. CD133+PC chemotaxis was assessed towards vascular endothelial growth factor, an angiogenic stimulus upregulated in AMI. The expression of anti‐oxidant enzymes in CD133+PC was detected by reverse‐transcriptase PCR.
Results. In non‐DM patients, the number of CD133+PC increased on day 3 following AMI (P = 0.0001). In contrast, no changes were observed in AMI patients with T2DM. Regarding the function of CD133+PC, an enhanced chemotactic response was observed following AMI in both non‐DM (P = 0.0001) and T2DM (P = 0.007). However, the AMI‐related functional activation was significantly weaker in diabetic patients (P = 0.001). Moreover, the expression of catalase was lower in CD133+PC from T2DM.
Conclusions. Our results show that T2DM not only limits the abundance of CD133+PC following AMI, but also limits their activation. This might be explained by a lower resistance of CD133+PC to oxidative stress. Our data provide a possible explanation for the delayed postischaemic vascular healing and myocardial recovery in DM.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>19019194</pmid><doi>10.1111/j.1365-2796.2008.02011.x</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | AC133 Antigen acute myocardial infarction Aged Antigens, CD Biological and medical sciences Biomarkers CD133 Chemotaxis - physiology coronary heart disease diabetes mellitus Diabetes Mellitus, Type 2 - blood Diabetes. Impaired glucose tolerance Diabetic Angiopathies - blood Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Flow Cytometry General aspects Glycoproteins Humans Male Medical sciences Middle Aged Myocardial Infarction - blood Myocardial Infarction - pathology Peptides Pilot Projects progenitor cells Prospective Studies Stem Cells - physiology Vascular Endothelial Growth Factor Receptor-1 - blood |
| title | Diabetes mellitus impairs CD133+ progenitor cell function after myocardial infarction |
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