The functional polymorphism rs73598374:G>A (p.Asp8Asn) of the ADA gene is associated with telomerase activity and leukocyte telomere length
Recent evidence demonstrated a relevant role of adenosine deaminase (ADA) in replicative senescence of T cells through its capacity to modulate telomerase activity (TA). Herein, we tested the impact of the functional polymorphism ADA rs73598374:G>A (c.22G>A, p.Asp8Asn) on telomere biology, by...
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| Veröffentlicht in: | European journal of human genetics : EJHG 2015-02, Vol.23 (2), p.267-270 |
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| creator | Concetti, Fabio Carpi, Francesco M Nabissi, Massimo Picciolini, Matteo Santoni, Giorgio Napolioni, Valerio |
| description | Recent evidence demonstrated a relevant role of adenosine deaminase (ADA) in replicative senescence of T cells through its capacity to modulate telomerase activity (TA). Herein, we tested the impact of the functional polymorphism ADA rs73598374:G>A (c.22G>A, p.Asp8Asn) on telomere biology, by measuring TA and leukocyte telomere length (LTL) in healthy subjects selected according to rs73598374 genotype. rs73598374-A carriers showed lower TA (P=0.019) and shorter LTL (P=0.003), respectively, compared to G/G carriers. rs73598374-A carriers showed a stronger cross-sectional age reduction of LTL (r=-0.314, P=0.005) compared to G/G carriers (r=-0.243, P=0.022). The reduced ADA activity associated to rs73598374-A variant predisposes those carriers to display higher levels of adenosine compared to G/G carriers. Consequently, it may lead to an accelerated process of replicative senescence, causing a stronger reduction of TA and in turn shorter LTL. In conclusion, the crucial role played by replicative senescence of the immune system in several human diseases and in the aging process underscores the relevance of the present findings and also spurs interest into the possible involvement of rs73598374 in shaping the susceptibility to several age-related diseases. |
| doi_str_mv | 10.1038/ejhg.2014.102 |
| format | Article |
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Herein, we tested the impact of the functional polymorphism ADA rs73598374:G>A (c.22G>A, p.Asp8Asn) on telomere biology, by measuring TA and leukocyte telomere length (LTL) in healthy subjects selected according to rs73598374 genotype. rs73598374-A carriers showed lower TA (P=0.019) and shorter LTL (P=0.003), respectively, compared to G/G carriers. rs73598374-A carriers showed a stronger cross-sectional age reduction of LTL (r=-0.314, P=0.005) compared to G/G carriers (r=-0.243, P=0.022). The reduced ADA activity associated to rs73598374-A variant predisposes those carriers to display higher levels of adenosine compared to G/G carriers. Consequently, it may lead to an accelerated process of replicative senescence, causing a stronger reduction of TA and in turn shorter LTL. In conclusion, the crucial role played by replicative senescence of the immune system in several human diseases and in the aging process underscores the relevance of the present findings and also spurs interest into the possible involvement of rs73598374 in shaping the susceptibility to several age-related diseases.</description><identifier>ISSN: 1018-4813</identifier><identifier>EISSN: 1476-5438</identifier><identifier>DOI: 10.1038/ejhg.2014.102</identifier><identifier>PMID: 24896148</identifier><language>eng</language><publisher>England: Nature Publishing Group</publisher><subject>Acquired immune deficiency syndrome ; ADA gene ; Adenosine ; Adenosine deaminase ; Adenosine Deaminase - genetics ; Adenosine Deaminase - metabolism ; Adult ; Age ; Aged ; Aged, 80 and over ; Aging ; AIDS ; Biology ; Cell culture ; Chromosomes ; Female ; Gene polymorphism ; Genetics ; Genomics ; Genotype & phenotype ; Humans ; Immune system ; Immunology ; Leukocytes - metabolism ; Lymphocytes ; Lymphocytes T ; Male ; Polymorphism, Single Nucleotide ; Senescence ; Short Report ; Telomerase ; Telomerase - metabolism ; Telomere Homeostasis - genetics</subject><ispartof>European journal of human genetics : EJHG, 2015-02, Vol.23 (2), p.267-270</ispartof><rights>Copyright Nature Publishing Group Feb 2015</rights><rights>Copyright © 2015 Macmillan Publishers Limited 2015 Macmillan Publishers Limited</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-d17d27def21b00885a4e8c847ecb8a3013d37c30a55540fa3c3fe5edc195001f3</citedby><cites>FETCH-LOGICAL-c448t-d17d27def21b00885a4e8c847ecb8a3013d37c30a55540fa3c3fe5edc195001f3</cites><orcidid>0000000243786838 ; 0000-0002-4378-6838</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4297891/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4297891/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24896148$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Concetti, Fabio</creatorcontrib><creatorcontrib>Carpi, Francesco M</creatorcontrib><creatorcontrib>Nabissi, Massimo</creatorcontrib><creatorcontrib>Picciolini, Matteo</creatorcontrib><creatorcontrib>Santoni, Giorgio</creatorcontrib><creatorcontrib>Napolioni, Valerio</creatorcontrib><title>The functional polymorphism rs73598374:G>A (p.Asp8Asn) of the ADA gene is associated with telomerase activity and leukocyte telomere length</title><title>European journal of human genetics : EJHG</title><addtitle>Eur J Hum Genet</addtitle><description>Recent evidence demonstrated a relevant role of adenosine deaminase (ADA) in replicative senescence of T cells through its capacity to modulate telomerase activity (TA). Herein, we tested the impact of the functional polymorphism ADA rs73598374:G>A (c.22G>A, p.Asp8Asn) on telomere biology, by measuring TA and leukocyte telomere length (LTL) in healthy subjects selected according to rs73598374 genotype. rs73598374-A carriers showed lower TA (P=0.019) and shorter LTL (P=0.003), respectively, compared to G/G carriers. rs73598374-A carriers showed a stronger cross-sectional age reduction of LTL (r=-0.314, P=0.005) compared to G/G carriers (r=-0.243, P=0.022). The reduced ADA activity associated to rs73598374-A variant predisposes those carriers to display higher levels of adenosine compared to G/G carriers. Consequently, it may lead to an accelerated process of replicative senescence, causing a stronger reduction of TA and in turn shorter LTL. In conclusion, the crucial role played by replicative senescence of the immune system in several human diseases and in the aging process underscores the relevance of the present findings and also spurs interest into the possible involvement of rs73598374 in shaping the susceptibility to several age-related diseases.</description><subject>Acquired immune deficiency syndrome</subject><subject>ADA gene</subject><subject>Adenosine</subject><subject>Adenosine deaminase</subject><subject>Adenosine Deaminase - genetics</subject><subject>Adenosine Deaminase - metabolism</subject><subject>Adult</subject><subject>Age</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Aging</subject><subject>AIDS</subject><subject>Biology</subject><subject>Cell culture</subject><subject>Chromosomes</subject><subject>Female</subject><subject>Gene polymorphism</subject><subject>Genetics</subject><subject>Genomics</subject><subject>Genotype & phenotype</subject><subject>Humans</subject><subject>Immune system</subject><subject>Immunology</subject><subject>Leukocytes - metabolism</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Male</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Senescence</subject><subject>Short Report</subject><subject>Telomerase</subject><subject>Telomerase - metabolism</subject><subject>Telomere Homeostasis - genetics</subject><issn>1018-4813</issn><issn>1476-5438</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkk1v1DAQhi0EomXhyBVZ4lIOWfy59nKoFBUoSJW4lLPldSYbL0kcbKfV_gb-NI76IeDEaTzjZ17N2C9CrylZU8L1ezh0-zUjVJSUPUGnVKhNJQXXT8uZUF0JTfkJepHSgRRKKfocnTChtxsq9Cn6dd0BbufRZR9G2-Mp9MchxKnzacAxKS63mivx4fK8xmfTuk6TrtP4DocW59JZf6zxHkbAPmGbUnDeZmjwrc8dztCHAaJNgG2Rv_H5iO3Y4B7mH8EdMzwQUErjPncv0bPW9gle3ccV-v750_XFl-rq2-XXi_qqckLoXDVUNUw10DK6I0RraQVop4UCt9OWE8obrhwnVkopSGu54y1IaBzdyvIELV-h8zvdad4NpQ5jjrY3U_SDjUcTrDd_34y-M_twYwTbKr2lReDsXiCGnzOkbAafHPS9HSHMydDNRjCihJD_gUrGNWGMF_TtP-ghzLF8ykIJKZWShV2h6o5yMaQUoX2cmxKzOMIsjjCLI0q68G_-XPaRfrAA_w144bIH</recordid><startdate>20150201</startdate><enddate>20150201</enddate><creator>Concetti, Fabio</creator><creator>Carpi, Francesco M</creator><creator>Nabissi, Massimo</creator><creator>Picciolini, Matteo</creator><creator>Santoni, Giorgio</creator><creator>Napolioni, Valerio</creator><general>Nature Publishing Group</general><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>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000000243786838</orcidid><orcidid>https://orcid.org/0000-0002-4378-6838</orcidid></search><sort><creationdate>20150201</creationdate><title>The functional polymorphism rs73598374:G>A (p.Asp8Asn) of the ADA gene is associated with telomerase activity and leukocyte telomere length</title><author>Concetti, Fabio ; Carpi, Francesco M ; Nabissi, Massimo ; Picciolini, Matteo ; Santoni, Giorgio ; Napolioni, Valerio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-d17d27def21b00885a4e8c847ecb8a3013d37c30a55540fa3c3fe5edc195001f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Acquired immune deficiency syndrome</topic><topic>ADA gene</topic><topic>Adenosine</topic><topic>Adenosine deaminase</topic><topic>Adenosine Deaminase - genetics</topic><topic>Adenosine Deaminase - metabolism</topic><topic>Adult</topic><topic>Age</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Aging</topic><topic>AIDS</topic><topic>Biology</topic><topic>Cell culture</topic><topic>Chromosomes</topic><topic>Female</topic><topic>Gene polymorphism</topic><topic>Genetics</topic><topic>Genomics</topic><topic>Genotype & phenotype</topic><topic>Humans</topic><topic>Immune system</topic><topic>Immunology</topic><topic>Leukocytes - metabolism</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Male</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Senescence</topic><topic>Short Report</topic><topic>Telomerase</topic><topic>Telomerase - metabolism</topic><topic>Telomere Homeostasis - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Concetti, Fabio</creatorcontrib><creatorcontrib>Carpi, Francesco M</creatorcontrib><creatorcontrib>Nabissi, Massimo</creatorcontrib><creatorcontrib>Picciolini, Matteo</creatorcontrib><creatorcontrib>Santoni, Giorgio</creatorcontrib><creatorcontrib>Napolioni, Valerio</creatorcontrib><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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>European journal of human genetics : EJHG</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Concetti, Fabio</au><au>Carpi, Francesco M</au><au>Nabissi, Massimo</au><au>Picciolini, Matteo</au><au>Santoni, Giorgio</au><au>Napolioni, Valerio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The functional polymorphism rs73598374:G>A (p.Asp8Asn) of the ADA gene is associated with telomerase activity and leukocyte telomere length</atitle><jtitle>European journal of human genetics : EJHG</jtitle><addtitle>Eur J Hum Genet</addtitle><date>2015-02-01</date><risdate>2015</risdate><volume>23</volume><issue>2</issue><spage>267</spage><epage>270</epage><pages>267-270</pages><issn>1018-4813</issn><eissn>1476-5438</eissn><abstract>Recent evidence demonstrated a relevant role of adenosine deaminase (ADA) in replicative senescence of T cells through its capacity to modulate telomerase activity (TA). Herein, we tested the impact of the functional polymorphism ADA rs73598374:G>A (c.22G>A, p.Asp8Asn) on telomere biology, by measuring TA and leukocyte telomere length (LTL) in healthy subjects selected according to rs73598374 genotype. rs73598374-A carriers showed lower TA (P=0.019) and shorter LTL (P=0.003), respectively, compared to G/G carriers. rs73598374-A carriers showed a stronger cross-sectional age reduction of LTL (r=-0.314, P=0.005) compared to G/G carriers (r=-0.243, P=0.022). The reduced ADA activity associated to rs73598374-A variant predisposes those carriers to display higher levels of adenosine compared to G/G carriers. Consequently, it may lead to an accelerated process of replicative senescence, causing a stronger reduction of TA and in turn shorter LTL. In conclusion, the crucial role played by replicative senescence of the immune system in several human diseases and in the aging process underscores the relevance of the present findings and also spurs interest into the possible involvement of rs73598374 in shaping the susceptibility to several age-related diseases.</abstract><cop>England</cop><pub>Nature Publishing Group</pub><pmid>24896148</pmid><doi>10.1038/ejhg.2014.102</doi><tpages>4</tpages><orcidid>https://orcid.org/0000000243786838</orcidid><orcidid>https://orcid.org/0000-0002-4378-6838</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Acquired immune deficiency syndrome ADA gene Adenosine Adenosine deaminase Adenosine Deaminase - genetics Adenosine Deaminase - metabolism Adult Age Aged Aged, 80 and over Aging AIDS Biology Cell culture Chromosomes Female Gene polymorphism Genetics Genomics Genotype & phenotype Humans Immune system Immunology Leukocytes - metabolism Lymphocytes Lymphocytes T Male Polymorphism, Single Nucleotide Senescence Short Report Telomerase Telomerase - metabolism Telomere Homeostasis - genetics |
| title | The functional polymorphism rs73598374:G>A (p.Asp8Asn) of the ADA gene is associated with telomerase activity and leukocyte telomere length |
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