Alteration of Adenosine Receptors in Patients with Chronic Obstructive Pulmonary Disease
Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of mortality worldwide. Adenosine is an inflammatory regulator that acts through four distinct receptors to mediate pro- and antiinflammatory effects. The primary aim of this study was to investigate the expression, affinity, a...
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| Veröffentlicht in: | American journal of respiratory and critical care medicine 2006-02, Vol.173 (4), p.398-406 |
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| creator | Varani, Katia Caramori, Gaetano Vincenzi, Fabrizio Adcock, Ian Casolari, Paolo Leung, Edward MacLennan, Stephen Gessi, Stefania Morello, Silvana Barnes, Peter J Ito, Kazuhiro Chung, Kian Fan Cavallesco, Giorgio Azzena, Gianfranco Papi, Alberto Borea, Pier Andrea |
| description | Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of mortality worldwide. Adenosine is an inflammatory regulator that acts through four distinct receptors to mediate pro- and antiinflammatory effects.
The primary aim of this study was to investigate the expression, affinity, and density of adenosine receptors in peripheral lung parenchyma from age-matched smokers with COPD (n = 14) and smokers with normal lung function (control group; n = 20).
Adenosine receptors were analyzed by immunohistochemistry and saturation binding assays using typical antagonist radioligands.
A(1), A(2A), A(2B), and A(3) receptors were expressed in different cells in peripheral lung parenchyma. The affinity of A(1), A(2A), and A(3) receptors was significantly decreased in patients with COPD compared with the control group (K(D)[A(1)] = 3.15 +/- 0.19 vs. 1.70 +/- 0.14 nM; K(D)[A(2A)] = 7.88 +/- 0.68 vs. 1.87 +/- 0.09 nM; K(D)[A(3)] = 9.34 +/- 0.27 vs. 4.41 +/- 0.25 nM; p < 0.01), whereas their density was increased (Bmax[A(1)] = 53 +/- 4 vs. 32 +/- 3 fmol/mg protein; Bmax[A(2A)] = 852 +/- 50 vs. 302 +/- 12 fmol/mg protein; Bmax[A(3)] = 2,078 +/- 108 vs. 770 +/- 34 fmol/mg protein; p < 0.01). The affinity of A(2B) receptors was not altered, but the density was significantly decreased in patients with COPD compared with the control group (Bmax = 66 +/- 5 vs. 189 +/- 16 fmol/mg protein; p < 0.01). A significant correlation was found between the affinity and density of the adenosine receptors and the FEV(1)/FVC ratio.
This is the first report showing the presence of adenosine receptors in lung parenchyma in subjects with COPD compared with control smokers. These novel findings strengthen the hypothesis of a potential role played by adenosine receptors in the pathogenesis of COPD. |
| doi_str_mv | 10.1164/rccm.200506-869OC |
| format | Article |
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The primary aim of this study was to investigate the expression, affinity, and density of adenosine receptors in peripheral lung parenchyma from age-matched smokers with COPD (n = 14) and smokers with normal lung function (control group; n = 20).
Adenosine receptors were analyzed by immunohistochemistry and saturation binding assays using typical antagonist radioligands.
A(1), A(2A), A(2B), and A(3) receptors were expressed in different cells in peripheral lung parenchyma. The affinity of A(1), A(2A), and A(3) receptors was significantly decreased in patients with COPD compared with the control group (K(D)[A(1)] = 3.15 +/- 0.19 vs. 1.70 +/- 0.14 nM; K(D)[A(2A)] = 7.88 +/- 0.68 vs. 1.87 +/- 0.09 nM; K(D)[A(3)] = 9.34 +/- 0.27 vs. 4.41 +/- 0.25 nM; p < 0.01), whereas their density was increased (Bmax[A(1)] = 53 +/- 4 vs. 32 +/- 3 fmol/mg protein; Bmax[A(2A)] = 852 +/- 50 vs. 302 +/- 12 fmol/mg protein; Bmax[A(3)] = 2,078 +/- 108 vs. 770 +/- 34 fmol/mg protein; p < 0.01). The affinity of A(2B) receptors was not altered, but the density was significantly decreased in patients with COPD compared with the control group (Bmax = 66 +/- 5 vs. 189 +/- 16 fmol/mg protein; p < 0.01). A significant correlation was found between the affinity and density of the adenosine receptors and the FEV(1)/FVC ratio.
This is the first report showing the presence of adenosine receptors in lung parenchyma in subjects with COPD compared with control smokers. These novel findings strengthen the hypothesis of a potential role played by adenosine receptors in the pathogenesis of COPD.</description><identifier>ISSN: 1073-449X</identifier><identifier>EISSN: 1535-4970</identifier><identifier>DOI: 10.1164/rccm.200506-869OC</identifier><identifier>PMID: 16322645</identifier><language>eng</language><publisher>New York, NY: Am Thoracic Soc</publisher><subject>Aged ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Biological and medical sciences ; Chronic obstructive pulmonary disease, asthma ; Female ; Humans ; Immunohistochemistry ; Intensive care medicine ; Lung - chemistry ; Lung - immunology ; Male ; Medical sciences ; Pneumology ; Pulmonary Disease, Chronic Obstructive - immunology ; Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases ; Receptors, Purinergic P1 - analysis ; Receptors, Purinergic P1 - biosynthesis</subject><ispartof>American journal of respiratory and critical care medicine, 2006-02, Vol.173 (4), p.398-406</ispartof><rights>2006 INIST-CNRS</rights><rights>Copyright American Thoracic Society Feb 15, 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-dc38445fc9303e1f6434784f4bd1606d50208712b00d312759ecde31054d3dc83</citedby><cites>FETCH-LOGICAL-c390t-dc38445fc9303e1f6434784f4bd1606d50208712b00d312759ecde31054d3dc83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,4011,4012,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17485310$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16322645$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Varani, Katia</creatorcontrib><creatorcontrib>Caramori, Gaetano</creatorcontrib><creatorcontrib>Vincenzi, Fabrizio</creatorcontrib><creatorcontrib>Adcock, Ian</creatorcontrib><creatorcontrib>Casolari, Paolo</creatorcontrib><creatorcontrib>Leung, Edward</creatorcontrib><creatorcontrib>MacLennan, Stephen</creatorcontrib><creatorcontrib>Gessi, Stefania</creatorcontrib><creatorcontrib>Morello, Silvana</creatorcontrib><creatorcontrib>Barnes, Peter J</creatorcontrib><creatorcontrib>Ito, Kazuhiro</creatorcontrib><creatorcontrib>Chung, Kian Fan</creatorcontrib><creatorcontrib>Cavallesco, Giorgio</creatorcontrib><creatorcontrib>Azzena, Gianfranco</creatorcontrib><creatorcontrib>Papi, Alberto</creatorcontrib><creatorcontrib>Borea, Pier Andrea</creatorcontrib><title>Alteration of Adenosine Receptors in Patients with Chronic Obstructive Pulmonary Disease</title><title>American journal of respiratory and critical care medicine</title><addtitle>Am J Respir Crit Care Med</addtitle><description>Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of mortality worldwide. Adenosine is an inflammatory regulator that acts through four distinct receptors to mediate pro- and antiinflammatory effects.
The primary aim of this study was to investigate the expression, affinity, and density of adenosine receptors in peripheral lung parenchyma from age-matched smokers with COPD (n = 14) and smokers with normal lung function (control group; n = 20).
Adenosine receptors were analyzed by immunohistochemistry and saturation binding assays using typical antagonist radioligands.
A(1), A(2A), A(2B), and A(3) receptors were expressed in different cells in peripheral lung parenchyma. The affinity of A(1), A(2A), and A(3) receptors was significantly decreased in patients with COPD compared with the control group (K(D)[A(1)] = 3.15 +/- 0.19 vs. 1.70 +/- 0.14 nM; K(D)[A(2A)] = 7.88 +/- 0.68 vs. 1.87 +/- 0.09 nM; K(D)[A(3)] = 9.34 +/- 0.27 vs. 4.41 +/- 0.25 nM; p < 0.01), whereas their density was increased (Bmax[A(1)] = 53 +/- 4 vs. 32 +/- 3 fmol/mg protein; Bmax[A(2A)] = 852 +/- 50 vs. 302 +/- 12 fmol/mg protein; Bmax[A(3)] = 2,078 +/- 108 vs. 770 +/- 34 fmol/mg protein; p < 0.01). The affinity of A(2B) receptors was not altered, but the density was significantly decreased in patients with COPD compared with the control group (Bmax = 66 +/- 5 vs. 189 +/- 16 fmol/mg protein; p < 0.01). A significant correlation was found between the affinity and density of the adenosine receptors and the FEV(1)/FVC ratio.
This is the first report showing the presence of adenosine receptors in lung parenchyma in subjects with COPD compared with control smokers. These novel findings strengthen the hypothesis of a potential role played by adenosine receptors in the pathogenesis of COPD.</description><subject>Aged</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Biological and medical sciences</subject><subject>Chronic obstructive pulmonary disease, asthma</subject><subject>Female</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Intensive care medicine</subject><subject>Lung - chemistry</subject><subject>Lung - immunology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Pneumology</subject><subject>Pulmonary Disease, Chronic Obstructive - immunology</subject><subject>Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases</subject><subject>Receptors, Purinergic P1 - analysis</subject><subject>Receptors, Purinergic P1 - biosynthesis</subject><issn>1073-449X</issn><issn>1535-4970</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpd0MuKFDEUBuBCFGccfQA3EgQFFzWeVG5Vy6a9wkAPojC7kE5O2WmqkjZJOfj2pu2GAVfJ4jt_cv6meUnhmlLJ3ydr5-sOQIBsezls1o-aSyqYaPmg4HG9g2It58PdRfMs5z0A7XoKT5sLKlnXSS4um7vVVDCZ4mMgcSQrhyFmH5B8Q4uHElMmPpDbCjCUTO592ZH1LsXgLdlsc0mLLf43kttlmmMw6Q_54DOajM-bJ6OZMr44n1fNj08fv6-_tDebz1_Xq5vWsgFK6yzrORejHRgwpKPkjKuej3zrqATpBHTQK9ptARyjnRIDWoeMguCOOduzq-btKfeQ4q8Fc9GzzxanyQSMS9ZSSQ5CqApf_wf3cUmh_k3TYZBcdoJXRE_IpphzwlEfkp_rWpqCPnauj53rU-f6X-d15tU5eNnO6B4mziVX8OYMTLZmGpMJ1ucHp3gv6kbVvTu5nf-5u_cJdZ7NNNVYqs3--DBVTHPNhp79BYPQmBk</recordid><startdate>20060215</startdate><enddate>20060215</enddate><creator>Varani, Katia</creator><creator>Caramori, Gaetano</creator><creator>Vincenzi, Fabrizio</creator><creator>Adcock, Ian</creator><creator>Casolari, Paolo</creator><creator>Leung, Edward</creator><creator>MacLennan, Stephen</creator><creator>Gessi, Stefania</creator><creator>Morello, Silvana</creator><creator>Barnes, Peter J</creator><creator>Ito, Kazuhiro</creator><creator>Chung, Kian Fan</creator><creator>Cavallesco, Giorgio</creator><creator>Azzena, Gianfranco</creator><creator>Papi, Alberto</creator><creator>Borea, Pier Andrea</creator><general>Am Thoracic Soc</general><general>American Lung Association</general><general>American Thoracic Society</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>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20060215</creationdate><title>Alteration of Adenosine Receptors in Patients with Chronic Obstructive Pulmonary Disease</title><author>Varani, Katia ; Caramori, Gaetano ; Vincenzi, Fabrizio ; Adcock, Ian ; Casolari, Paolo ; Leung, Edward ; MacLennan, Stephen ; Gessi, Stefania ; Morello, Silvana ; Barnes, Peter J ; Ito, Kazuhiro ; Chung, Kian Fan ; Cavallesco, Giorgio ; Azzena, Gianfranco ; Papi, Alberto ; Borea, Pier Andrea</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-dc38445fc9303e1f6434784f4bd1606d50208712b00d312759ecde31054d3dc83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Aged</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Biological and medical sciences</topic><topic>Chronic obstructive pulmonary disease, asthma</topic><topic>Female</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Intensive care medicine</topic><topic>Lung - chemistry</topic><topic>Lung - immunology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Pneumology</topic><topic>Pulmonary Disease, Chronic Obstructive - immunology</topic><topic>Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases</topic><topic>Receptors, Purinergic P1 - analysis</topic><topic>Receptors, Purinergic P1 - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Varani, Katia</creatorcontrib><creatorcontrib>Caramori, Gaetano</creatorcontrib><creatorcontrib>Vincenzi, Fabrizio</creatorcontrib><creatorcontrib>Adcock, Ian</creatorcontrib><creatorcontrib>Casolari, Paolo</creatorcontrib><creatorcontrib>Leung, Edward</creatorcontrib><creatorcontrib>MacLennan, Stephen</creatorcontrib><creatorcontrib>Gessi, Stefania</creatorcontrib><creatorcontrib>Morello, Silvana</creatorcontrib><creatorcontrib>Barnes, Peter J</creatorcontrib><creatorcontrib>Ito, Kazuhiro</creatorcontrib><creatorcontrib>Chung, Kian Fan</creatorcontrib><creatorcontrib>Cavallesco, Giorgio</creatorcontrib><creatorcontrib>Azzena, Gianfranco</creatorcontrib><creatorcontrib>Papi, Alberto</creatorcontrib><creatorcontrib>Borea, Pier Andrea</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>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of respiratory and critical care medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Varani, Katia</au><au>Caramori, Gaetano</au><au>Vincenzi, Fabrizio</au><au>Adcock, Ian</au><au>Casolari, Paolo</au><au>Leung, Edward</au><au>MacLennan, Stephen</au><au>Gessi, Stefania</au><au>Morello, Silvana</au><au>Barnes, Peter J</au><au>Ito, Kazuhiro</au><au>Chung, Kian Fan</au><au>Cavallesco, Giorgio</au><au>Azzena, Gianfranco</au><au>Papi, Alberto</au><au>Borea, Pier Andrea</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Alteration of Adenosine Receptors in Patients with Chronic Obstructive Pulmonary Disease</atitle><jtitle>American journal of respiratory and critical care medicine</jtitle><addtitle>Am J Respir Crit Care Med</addtitle><date>2006-02-15</date><risdate>2006</risdate><volume>173</volume><issue>4</issue><spage>398</spage><epage>406</epage><pages>398-406</pages><issn>1073-449X</issn><eissn>1535-4970</eissn><abstract>Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of mortality worldwide. Adenosine is an inflammatory regulator that acts through four distinct receptors to mediate pro- and antiinflammatory effects.
The primary aim of this study was to investigate the expression, affinity, and density of adenosine receptors in peripheral lung parenchyma from age-matched smokers with COPD (n = 14) and smokers with normal lung function (control group; n = 20).
Adenosine receptors were analyzed by immunohistochemistry and saturation binding assays using typical antagonist radioligands.
A(1), A(2A), A(2B), and A(3) receptors were expressed in different cells in peripheral lung parenchyma. The affinity of A(1), A(2A), and A(3) receptors was significantly decreased in patients with COPD compared with the control group (K(D)[A(1)] = 3.15 +/- 0.19 vs. 1.70 +/- 0.14 nM; K(D)[A(2A)] = 7.88 +/- 0.68 vs. 1.87 +/- 0.09 nM; K(D)[A(3)] = 9.34 +/- 0.27 vs. 4.41 +/- 0.25 nM; p < 0.01), whereas their density was increased (Bmax[A(1)] = 53 +/- 4 vs. 32 +/- 3 fmol/mg protein; Bmax[A(2A)] = 852 +/- 50 vs. 302 +/- 12 fmol/mg protein; Bmax[A(3)] = 2,078 +/- 108 vs. 770 +/- 34 fmol/mg protein; p < 0.01). The affinity of A(2B) receptors was not altered, but the density was significantly decreased in patients with COPD compared with the control group (Bmax = 66 +/- 5 vs. 189 +/- 16 fmol/mg protein; p < 0.01). A significant correlation was found between the affinity and density of the adenosine receptors and the FEV(1)/FVC ratio.
This is the first report showing the presence of adenosine receptors in lung parenchyma in subjects with COPD compared with control smokers. These novel findings strengthen the hypothesis of a potential role played by adenosine receptors in the pathogenesis of COPD.</abstract><cop>New York, NY</cop><pub>Am Thoracic Soc</pub><pmid>16322645</pmid><doi>10.1164/rccm.200506-869OC</doi><tpages>9</tpages></addata></record> |
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| source | MEDLINE; American Thoracic Society (ATS) Journals Online; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection; Journals@Ovid Complete |
| subjects | Aged Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Biological and medical sciences Chronic obstructive pulmonary disease, asthma Female Humans Immunohistochemistry Intensive care medicine Lung - chemistry Lung - immunology Male Medical sciences Pneumology Pulmonary Disease, Chronic Obstructive - immunology Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases Receptors, Purinergic P1 - analysis Receptors, Purinergic P1 - biosynthesis |
| title | Alteration of Adenosine Receptors in Patients with Chronic Obstructive Pulmonary Disease |
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