Galectin‐3, a Biomarker Linking Oxidative Stress and Inflammation With the Clinical Outcomes of Patients With Atherothrombosis
Background Galectin‐3 (Gal‐3) participates in different mechanisms involved in atherothrombosis, such as inflammation, proliferation, or macrophage chemotaxis. Thus, there have been committed intensive efforts to elucidate the function of Gal‐3 in cardiovascular (CV) diseases. The role of Gal‐3 as a...
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| Veröffentlicht in: | Journal of the American Heart Association 2014-08, Vol.3 (4), p.n/a |
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| creator | Madrigal‐Matute, Julio Lindholt, Jes Sandal Fernandez‐Garcia, Carlos Ernesto Benito‐Martin, Alberto Burillo, Elena Zalba, Guillermo Beloqui, Oscar Llamas‐Granda, Patricia Ortiz, Alberto Egido, Jesus Blanco‐Colio, Luis Miguel Martin‐Ventura, Jose Luis |
| description | Background
Galectin‐3 (Gal‐3) participates in different mechanisms involved in atherothrombosis, such as inflammation, proliferation, or macrophage chemotaxis. Thus, there have been committed intensive efforts to elucidate the function of Gal‐3 in cardiovascular (CV) diseases. The role of Gal‐3 as a circulating biomarker has been demonstrated in patients with heart failure, but its importance as a biomarker in atherothrombosis is still unknown.
Methods and Results
Because Gal‐3 is involved in monocyte‐to‐macrophage transition, we used fresh isolated monocytes and the in vitro model of macrophage differentiation of THP‐1 cells stimulated with phorbol myristate acetate (PMA). Gal‐3 release is increased by PMA in human monocytes and macrophages, a process involving exosomes and regulated by reactive oxygen species/NADPH oxidase activity. In asymptomatic subjects (n=199), Gal‐3 plasma levels are correlated with NADPH oxidase activity in peripheral blood mononuclear cells (r=0.476; P |
| doi_str_mv | 10.1161/JAHA.114.000785 |
| format | Article |
| fullrecord | <record><control><sourceid>wiley_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4310363</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>JAH3627</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4387-e7ee5b07db4cbca758553f3edc5830ab10dbbf84859043ec1ce57c91249367a53</originalsourceid><addsrcrecordid>eNqFkU1OAyEAhYnRqKmu3RkOYCsMUGY2JmPjb5rURI3LCcMwLXYGGqDV7jyCZ_Qk0owaXbniAd97_DwAjjAaYDzEp7f5dR4VHSCEeMq2wH6CKO9nWYq2f-k9cOj9c2TQMOGEZbtgL2EoYylH--DtSjRKBm0-3t7JCRTwXNtWuLlycKzNXJspnLzqSgS9UvA-OOU9FKaCN6ZuRNvGdWvgkw4zGGYKjhpttBQNnCyDtK3y0NbwLkLKBN9heeScDTNn29J67Q_ATi0arw6_xh54vLx4GF33x5Orm1E-7ktKUt5XXClWIl6VVJZScJYyRmqiKslSgkSJUVWWdUpTliFKlMRSMS4znNCMDLlgpAfOutzFsmyjLd7IiaZYOB2fuy6s0MXfHaNnxdSuCkowIkMSA067AOms907VP16Mik0fxaaPqGjR9REdx7-P_OG_fz8CtANedKPW_-Vt5mRT4SeIJ5lw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Galectin‐3, a Biomarker Linking Oxidative Stress and Inflammation With the Clinical Outcomes of Patients With Atherothrombosis</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Wiley Online Library (Open Access Collection)</source><source>PubMed Central</source><creator>Madrigal‐Matute, Julio ; Lindholt, Jes Sandal ; Fernandez‐Garcia, Carlos Ernesto ; Benito‐Martin, Alberto ; Burillo, Elena ; Zalba, Guillermo ; Beloqui, Oscar ; Llamas‐Granda, Patricia ; Ortiz, Alberto ; Egido, Jesus ; Blanco‐Colio, Luis Miguel ; Martin‐Ventura, Jose Luis</creator><creatorcontrib>Madrigal‐Matute, Julio ; Lindholt, Jes Sandal ; Fernandez‐Garcia, Carlos Ernesto ; Benito‐Martin, Alberto ; Burillo, Elena ; Zalba, Guillermo ; Beloqui, Oscar ; Llamas‐Granda, Patricia ; Ortiz, Alberto ; Egido, Jesus ; Blanco‐Colio, Luis Miguel ; Martin‐Ventura, Jose Luis</creatorcontrib><description>Background
Galectin‐3 (Gal‐3) participates in different mechanisms involved in atherothrombosis, such as inflammation, proliferation, or macrophage chemotaxis. Thus, there have been committed intensive efforts to elucidate the function of Gal‐3 in cardiovascular (CV) diseases. The role of Gal‐3 as a circulating biomarker has been demonstrated in patients with heart failure, but its importance as a biomarker in atherothrombosis is still unknown.
Methods and Results
Because Gal‐3 is involved in monocyte‐to‐macrophage transition, we used fresh isolated monocytes and the in vitro model of macrophage differentiation of THP‐1 cells stimulated with phorbol myristate acetate (PMA). Gal‐3 release is increased by PMA in human monocytes and macrophages, a process involving exosomes and regulated by reactive oxygen species/NADPH oxidase activity. In asymptomatic subjects (n=199), Gal‐3 plasma levels are correlated with NADPH oxidase activity in peripheral blood mononuclear cells (r=0.476; P<0.001) and carotid intima‐media thickness (r=0.438; P<0.001), a surrogate marker of atherosclerosis. Accordingly, Gal‐3 plasma concentrations are increased in patients with carotid atherosclerosis (n=158), compared to control subjects (n=115; 14.3 [10.7 to 16.9] vs. 10.4 [8.6 to 12.5] ng/mL; P<0.001). Finally, on a 5‐year follow‐up study in patients with peripheral artery disease, Gal‐3 concentrations are significantly and independently associated with an increased risk for CV mortality (hazard ratio=2.24, 95% confidence interval: 1.06 to 4.73, P<0.05).
Conclusions
Gal‐3 extracellular levels could reflect key underlying mechanisms involved in atherosclerosis etiology, development, and plaque rupture, such as inflammation, infiltration of circulating cells and oxidative stress. Moreover, circulating Gal‐3 concentrations are associated with clinical outcomes in patients with atherothrombosis.</description><identifier>ISSN: 2047-9980</identifier><identifier>EISSN: 2047-9980</identifier><identifier>DOI: 10.1161/JAHA.114.000785</identifier><identifier>PMID: 25095870</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Aged ; atherothrombosis ; Biomarkers ; Carotid Artery Diseases - blood ; Carotid Artery Diseases - diagnostic imaging ; Carotid Intima-Media Thickness ; Case-Control Studies ; Cell Line ; Female ; Follow-Up Studies ; Galectin 3 - blood ; Galectin 3 - drug effects ; Humans ; In Vitro Techniques ; Inflammation ; Macrophages ; Male ; Middle Aged ; Monocytes ; mortality ; NADPH Oxidases - metabolism ; Original Research ; Oxidative Stress ; Peripheral Arterial Disease - blood ; Peripheral Arterial Disease - mortality ; Prognosis ; Tetradecanoylphorbol Acetate - pharmacology</subject><ispartof>Journal of the American Heart Association, 2014-08, Vol.3 (4), p.n/a</ispartof><rights>2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.</rights><rights>2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4387-e7ee5b07db4cbca758553f3edc5830ab10dbbf84859043ec1ce57c91249367a53</citedby><cites>FETCH-LOGICAL-c4387-e7ee5b07db4cbca758553f3edc5830ab10dbbf84859043ec1ce57c91249367a53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4310363/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4310363/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,11562,27924,27925,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25095870$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Madrigal‐Matute, Julio</creatorcontrib><creatorcontrib>Lindholt, Jes Sandal</creatorcontrib><creatorcontrib>Fernandez‐Garcia, Carlos Ernesto</creatorcontrib><creatorcontrib>Benito‐Martin, Alberto</creatorcontrib><creatorcontrib>Burillo, Elena</creatorcontrib><creatorcontrib>Zalba, Guillermo</creatorcontrib><creatorcontrib>Beloqui, Oscar</creatorcontrib><creatorcontrib>Llamas‐Granda, Patricia</creatorcontrib><creatorcontrib>Ortiz, Alberto</creatorcontrib><creatorcontrib>Egido, Jesus</creatorcontrib><creatorcontrib>Blanco‐Colio, Luis Miguel</creatorcontrib><creatorcontrib>Martin‐Ventura, Jose Luis</creatorcontrib><title>Galectin‐3, a Biomarker Linking Oxidative Stress and Inflammation With the Clinical Outcomes of Patients With Atherothrombosis</title><title>Journal of the American Heart Association</title><addtitle>J Am Heart Assoc</addtitle><description>Background
Galectin‐3 (Gal‐3) participates in different mechanisms involved in atherothrombosis, such as inflammation, proliferation, or macrophage chemotaxis. Thus, there have been committed intensive efforts to elucidate the function of Gal‐3 in cardiovascular (CV) diseases. The role of Gal‐3 as a circulating biomarker has been demonstrated in patients with heart failure, but its importance as a biomarker in atherothrombosis is still unknown.
Methods and Results
Because Gal‐3 is involved in monocyte‐to‐macrophage transition, we used fresh isolated monocytes and the in vitro model of macrophage differentiation of THP‐1 cells stimulated with phorbol myristate acetate (PMA). Gal‐3 release is increased by PMA in human monocytes and macrophages, a process involving exosomes and regulated by reactive oxygen species/NADPH oxidase activity. In asymptomatic subjects (n=199), Gal‐3 plasma levels are correlated with NADPH oxidase activity in peripheral blood mononuclear cells (r=0.476; P<0.001) and carotid intima‐media thickness (r=0.438; P<0.001), a surrogate marker of atherosclerosis. Accordingly, Gal‐3 plasma concentrations are increased in patients with carotid atherosclerosis (n=158), compared to control subjects (n=115; 14.3 [10.7 to 16.9] vs. 10.4 [8.6 to 12.5] ng/mL; P<0.001). Finally, on a 5‐year follow‐up study in patients with peripheral artery disease, Gal‐3 concentrations are significantly and independently associated with an increased risk for CV mortality (hazard ratio=2.24, 95% confidence interval: 1.06 to 4.73, P<0.05).
Conclusions
Gal‐3 extracellular levels could reflect key underlying mechanisms involved in atherosclerosis etiology, development, and plaque rupture, such as inflammation, infiltration of circulating cells and oxidative stress. Moreover, circulating Gal‐3 concentrations are associated with clinical outcomes in patients with atherothrombosis.</description><subject>Aged</subject><subject>atherothrombosis</subject><subject>Biomarkers</subject><subject>Carotid Artery Diseases - blood</subject><subject>Carotid Artery Diseases - diagnostic imaging</subject><subject>Carotid Intima-Media Thickness</subject><subject>Case-Control Studies</subject><subject>Cell Line</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Galectin 3 - blood</subject><subject>Galectin 3 - drug effects</subject><subject>Humans</subject><subject>In Vitro Techniques</subject><subject>Inflammation</subject><subject>Macrophages</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Monocytes</subject><subject>mortality</subject><subject>NADPH Oxidases - metabolism</subject><subject>Original Research</subject><subject>Oxidative Stress</subject><subject>Peripheral Arterial Disease - blood</subject><subject>Peripheral Arterial Disease - mortality</subject><subject>Prognosis</subject><subject>Tetradecanoylphorbol Acetate - pharmacology</subject><issn>2047-9980</issn><issn>2047-9980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><recordid>eNqFkU1OAyEAhYnRqKmu3RkOYCsMUGY2JmPjb5rURI3LCcMwLXYGGqDV7jyCZ_Qk0owaXbniAd97_DwAjjAaYDzEp7f5dR4VHSCEeMq2wH6CKO9nWYq2f-k9cOj9c2TQMOGEZbtgL2EoYylH--DtSjRKBm0-3t7JCRTwXNtWuLlycKzNXJspnLzqSgS9UvA-OOU9FKaCN6ZuRNvGdWvgkw4zGGYKjhpttBQNnCyDtK3y0NbwLkLKBN9heeScDTNn29J67Q_ATi0arw6_xh54vLx4GF33x5Orm1E-7ktKUt5XXClWIl6VVJZScJYyRmqiKslSgkSJUVWWdUpTliFKlMRSMS4znNCMDLlgpAfOutzFsmyjLd7IiaZYOB2fuy6s0MXfHaNnxdSuCkowIkMSA067AOms907VP16Mik0fxaaPqGjR9REdx7-P_OG_fz8CtANedKPW_-Vt5mRT4SeIJ5lw</recordid><startdate>20140805</startdate><enddate>20140805</enddate><creator>Madrigal‐Matute, Julio</creator><creator>Lindholt, Jes Sandal</creator><creator>Fernandez‐Garcia, Carlos Ernesto</creator><creator>Benito‐Martin, Alberto</creator><creator>Burillo, Elena</creator><creator>Zalba, Guillermo</creator><creator>Beloqui, Oscar</creator><creator>Llamas‐Granda, Patricia</creator><creator>Ortiz, Alberto</creator><creator>Egido, Jesus</creator><creator>Blanco‐Colio, Luis Miguel</creator><creator>Martin‐Ventura, Jose Luis</creator><general>Blackwell Publishing Ltd</general><scope>24P</scope><scope>WIN</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>5PM</scope></search><sort><creationdate>20140805</creationdate><title>Galectin‐3, a Biomarker Linking Oxidative Stress and Inflammation With the Clinical Outcomes of Patients With Atherothrombosis</title><author>Madrigal‐Matute, Julio ; Lindholt, Jes Sandal ; Fernandez‐Garcia, Carlos Ernesto ; Benito‐Martin, Alberto ; Burillo, Elena ; Zalba, Guillermo ; Beloqui, Oscar ; Llamas‐Granda, Patricia ; Ortiz, Alberto ; Egido, Jesus ; Blanco‐Colio, Luis Miguel ; Martin‐Ventura, Jose Luis</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4387-e7ee5b07db4cbca758553f3edc5830ab10dbbf84859043ec1ce57c91249367a53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Aged</topic><topic>atherothrombosis</topic><topic>Biomarkers</topic><topic>Carotid Artery Diseases - blood</topic><topic>Carotid Artery Diseases - diagnostic imaging</topic><topic>Carotid Intima-Media Thickness</topic><topic>Case-Control Studies</topic><topic>Cell Line</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Galectin 3 - blood</topic><topic>Galectin 3 - drug effects</topic><topic>Humans</topic><topic>In Vitro Techniques</topic><topic>Inflammation</topic><topic>Macrophages</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Monocytes</topic><topic>mortality</topic><topic>NADPH Oxidases - metabolism</topic><topic>Original Research</topic><topic>Oxidative Stress</topic><topic>Peripheral Arterial Disease - blood</topic><topic>Peripheral Arterial Disease - mortality</topic><topic>Prognosis</topic><topic>Tetradecanoylphorbol Acetate - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Madrigal‐Matute, Julio</creatorcontrib><creatorcontrib>Lindholt, Jes Sandal</creatorcontrib><creatorcontrib>Fernandez‐Garcia, Carlos Ernesto</creatorcontrib><creatorcontrib>Benito‐Martin, Alberto</creatorcontrib><creatorcontrib>Burillo, Elena</creatorcontrib><creatorcontrib>Zalba, Guillermo</creatorcontrib><creatorcontrib>Beloqui, Oscar</creatorcontrib><creatorcontrib>Llamas‐Granda, Patricia</creatorcontrib><creatorcontrib>Ortiz, Alberto</creatorcontrib><creatorcontrib>Egido, Jesus</creatorcontrib><creatorcontrib>Blanco‐Colio, Luis Miguel</creatorcontrib><creatorcontrib>Martin‐Ventura, Jose Luis</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library Free Content</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of the American Heart Association</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Madrigal‐Matute, Julio</au><au>Lindholt, Jes Sandal</au><au>Fernandez‐Garcia, Carlos Ernesto</au><au>Benito‐Martin, Alberto</au><au>Burillo, Elena</au><au>Zalba, Guillermo</au><au>Beloqui, Oscar</au><au>Llamas‐Granda, Patricia</au><au>Ortiz, Alberto</au><au>Egido, Jesus</au><au>Blanco‐Colio, Luis Miguel</au><au>Martin‐Ventura, Jose Luis</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Galectin‐3, a Biomarker Linking Oxidative Stress and Inflammation With the Clinical Outcomes of Patients With Atherothrombosis</atitle><jtitle>Journal of the American Heart Association</jtitle><addtitle>J Am Heart Assoc</addtitle><date>2014-08-05</date><risdate>2014</risdate><volume>3</volume><issue>4</issue><epage>n/a</epage><issn>2047-9980</issn><eissn>2047-9980</eissn><abstract>Background
Galectin‐3 (Gal‐3) participates in different mechanisms involved in atherothrombosis, such as inflammation, proliferation, or macrophage chemotaxis. Thus, there have been committed intensive efforts to elucidate the function of Gal‐3 in cardiovascular (CV) diseases. The role of Gal‐3 as a circulating biomarker has been demonstrated in patients with heart failure, but its importance as a biomarker in atherothrombosis is still unknown.
Methods and Results
Because Gal‐3 is involved in monocyte‐to‐macrophage transition, we used fresh isolated monocytes and the in vitro model of macrophage differentiation of THP‐1 cells stimulated with phorbol myristate acetate (PMA). Gal‐3 release is increased by PMA in human monocytes and macrophages, a process involving exosomes and regulated by reactive oxygen species/NADPH oxidase activity. In asymptomatic subjects (n=199), Gal‐3 plasma levels are correlated with NADPH oxidase activity in peripheral blood mononuclear cells (r=0.476; P<0.001) and carotid intima‐media thickness (r=0.438; P<0.001), a surrogate marker of atherosclerosis. Accordingly, Gal‐3 plasma concentrations are increased in patients with carotid atherosclerosis (n=158), compared to control subjects (n=115; 14.3 [10.7 to 16.9] vs. 10.4 [8.6 to 12.5] ng/mL; P<0.001). Finally, on a 5‐year follow‐up study in patients with peripheral artery disease, Gal‐3 concentrations are significantly and independently associated with an increased risk for CV mortality (hazard ratio=2.24, 95% confidence interval: 1.06 to 4.73, P<0.05).
Conclusions
Gal‐3 extracellular levels could reflect key underlying mechanisms involved in atherosclerosis etiology, development, and plaque rupture, such as inflammation, infiltration of circulating cells and oxidative stress. Moreover, circulating Gal‐3 concentrations are associated with clinical outcomes in patients with atherothrombosis.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>25095870</pmid><doi>10.1161/JAHA.114.000785</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged atherothrombosis Biomarkers Carotid Artery Diseases - blood Carotid Artery Diseases - diagnostic imaging Carotid Intima-Media Thickness Case-Control Studies Cell Line Female Follow-Up Studies Galectin 3 - blood Galectin 3 - drug effects Humans In Vitro Techniques Inflammation Macrophages Male Middle Aged Monocytes mortality NADPH Oxidases - metabolism Original Research Oxidative Stress Peripheral Arterial Disease - blood Peripheral Arterial Disease - mortality Prognosis Tetradecanoylphorbol Acetate - pharmacology |
| title | Galectin‐3, a Biomarker Linking Oxidative Stress and Inflammation With the Clinical Outcomes of Patients With Atherothrombosis |
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