Impaired genome maintenance suppresses the growth hormone--insulin-like growth factor 1 axis in mice with Cockayne syndrome
Cockayne syndrome (CS) is a photosensitive, DNA repair disorder associated with progeria that is caused by a defect in the transcription-coupled repair subpathway of nucleotide excision repair (NER). Here, complete inactivation of NER in Csb(m/m)/Xpa(-/-) mutants causes a phenotype that reliably mim...
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| Veröffentlicht in: | PLoS biology 2007-01, Vol.5 (1), p.e2-e2 |
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| creator | van der Pluijm, Ingrid Garinis, George A Brandt, Renata M C Gorgels, Theo G M F Wijnhoven, Susan W Diderich, Karin E M de Wit, Jan Mitchell, James R van Oostrom, Conny Beems, Rudolf Niedernhofer, Laura J Velasco, Susana Friedberg, Errol C Tanaka, Kiyoji van Steeg, Harry Hoeijmakers, Jan H J van der Horst, Gijsbertus T J |
| description | Cockayne syndrome (CS) is a photosensitive, DNA repair disorder associated with progeria that is caused by a defect in the transcription-coupled repair subpathway of nucleotide excision repair (NER). Here, complete inactivation of NER in Csb(m/m)/Xpa(-/-) mutants causes a phenotype that reliably mimics the human progeroid CS syndrome. Newborn Csb(m/m)/Xpa(-/-) mice display attenuated growth, progressive neurological dysfunction, retinal degeneration, cachexia, kyphosis, and die before weaning. Mouse liver transcriptome analysis and several physiological endpoints revealed systemic suppression of the growth hormone/insulin-like growth factor 1 (GH/IGF1) somatotroph axis and oxidative metabolism, increased antioxidant responses, and hypoglycemia together with hepatic glycogen and fat accumulation. Broad genome-wide parallels between Csb(m/m)/Xpa(-/-) and naturally aged mouse liver transcriptomes suggested that these changes are intrinsic to natural ageing and the DNA repair-deficient mice. Importantly, wild-type mice exposed to a low dose of chronic genotoxic stress recapitulated this response, thereby pointing to a novel link between genome instability and the age-related decline of the somatotroph axis. |
| doi_str_mv | 10.1371/journal.pbio.0050002 |
| format | Article |
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Here, complete inactivation of NER in Csb(m/m)/Xpa(-/-) mutants causes a phenotype that reliably mimics the human progeroid CS syndrome. Newborn Csb(m/m)/Xpa(-/-) mice display attenuated growth, progressive neurological dysfunction, retinal degeneration, cachexia, kyphosis, and die before weaning. Mouse liver transcriptome analysis and several physiological endpoints revealed systemic suppression of the growth hormone/insulin-like growth factor 1 (GH/IGF1) somatotroph axis and oxidative metabolism, increased antioxidant responses, and hypoglycemia together with hepatic glycogen and fat accumulation. Broad genome-wide parallels between Csb(m/m)/Xpa(-/-) and naturally aged mouse liver transcriptomes suggested that these changes are intrinsic to natural ageing and the DNA repair-deficient mice. Importantly, wild-type mice exposed to a low dose of chronic genotoxic stress recapitulated this response, thereby pointing to a novel link between genome instability and the age-related decline of the somatotroph axis.</description><identifier>ISSN: 1545-7885</identifier><identifier>ISSN: 1544-9173</identifier><identifier>EISSN: 1545-7885</identifier><identifier>DOI: 10.1371/journal.pbio.0050002</identifier><identifier>PMID: 17326724</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Age ; Aging ; Animals ; Antioxidants - pharmacology ; Cockayne syndrome ; Cockayne Syndrome - etiology ; Cockayne Syndrome - genetics ; Computational Biology ; Defects ; Deoxyribonucleic acid ; Diabetes and Endocrinology ; Diethylhexyl Phthalate - pharmacology ; DNA ; DNA damage ; DNA mismatch repair ; DNA Repair ; DNA Repair Enzymes - genetics ; DNA-Binding Proteins - genetics ; Experiments ; Fatty Acids - biosynthesis ; Genetic aspects ; Genetics and Genomics ; Genome - genetics ; Genomes ; Geriatrics ; Glucose - metabolism ; Growth Hormone - genetics ; Hypotheses ; Insulin-Like Growth Factor I - genetics ; Insulin-Like Growth Factor I - metabolism ; Insulin-like growth factors ; Liver - metabolism ; Male ; Mammals ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mus (Mouse) ; Oxidative stress ; Poly-ADP-Ribose Binding Proteins ; Proteins ; Radiation, Ionizing ; Rodents ; Somatotrophs - metabolism ; Xeroderma Pigmentosum Group A Protein - genetics</subject><ispartof>PLoS biology, 2007-01, Vol.5 (1), p.e2-e2</ispartof><rights>COPYRIGHT 2007 Public Library of Science</rights><rights>2007 van der Pluijm et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: van der Pluijm I, Garinis GA, Brandt RMC, Gorgels TGMF, Wijnhoven SW, et al. (2007) Impaired Genome Maintenance Suppresses the Growth Hormone-Insulin-Like Growth Factor 1 Axis in Mice with Cockayne Syndrome. 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Here, complete inactivation of NER in Csb(m/m)/Xpa(-/-) mutants causes a phenotype that reliably mimics the human progeroid CS syndrome. Newborn Csb(m/m)/Xpa(-/-) mice display attenuated growth, progressive neurological dysfunction, retinal degeneration, cachexia, kyphosis, and die before weaning. Mouse liver transcriptome analysis and several physiological endpoints revealed systemic suppression of the growth hormone/insulin-like growth factor 1 (GH/IGF1) somatotroph axis and oxidative metabolism, increased antioxidant responses, and hypoglycemia together with hepatic glycogen and fat accumulation. Broad genome-wide parallels between Csb(m/m)/Xpa(-/-) and naturally aged mouse liver transcriptomes suggested that these changes are intrinsic to natural ageing and the DNA repair-deficient mice. Importantly, wild-type mice exposed to a low dose of chronic genotoxic stress recapitulated this response, thereby pointing to a novel link between genome instability and the age-related decline of the somatotroph axis.</description><subject>Age</subject><subject>Aging</subject><subject>Animals</subject><subject>Antioxidants - pharmacology</subject><subject>Cockayne syndrome</subject><subject>Cockayne Syndrome - etiology</subject><subject>Cockayne Syndrome - genetics</subject><subject>Computational Biology</subject><subject>Defects</subject><subject>Deoxyribonucleic acid</subject><subject>Diabetes and Endocrinology</subject><subject>Diethylhexyl Phthalate - pharmacology</subject><subject>DNA</subject><subject>DNA damage</subject><subject>DNA mismatch repair</subject><subject>DNA Repair</subject><subject>DNA Repair Enzymes - genetics</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Experiments</subject><subject>Fatty Acids - biosynthesis</subject><subject>Genetic aspects</subject><subject>Genetics and Genomics</subject><subject>Genome - genetics</subject><subject>Genomes</subject><subject>Geriatrics</subject><subject>Glucose - metabolism</subject><subject>Growth Hormone - genetics</subject><subject>Hypotheses</subject><subject>Insulin-Like Growth Factor I - genetics</subject><subject>Insulin-Like Growth Factor I - metabolism</subject><subject>Insulin-like growth factors</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>Mammals</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mus (Mouse)</subject><subject>Oxidative stress</subject><subject>Poly-ADP-Ribose Binding Proteins</subject><subject>Proteins</subject><subject>Radiation, Ionizing</subject><subject>Rodents</subject><subject>Somatotrophs - metabolism</subject><subject>Xeroderma Pigmentosum Group A Protein - genetics</subject><issn>1545-7885</issn><issn>1544-9173</issn><issn>1545-7885</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</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><sourceid>DOA</sourceid><recordid>eNqVk1uL1DAUgIso7rr6D0QLguBDxyRNmuRFWAYvA4sL3l5DkqadzLZJTVp3B_-8GaeuO7Kg0oeWnO98pz2nJ8seQ7CAJYUvN34KTnaLQVm_AIAAANCd7BgSTArKGLl74_koexDjJgGII3Y_O4K0RBVF-Dj7vuoHaYOp89Y435u8l9aNxkmnTR6nYQgmRhPzcW3yNvjLcZ2vfei9M0VhXZw664rOXlwHG6lHH3KYyysbc-vy3ibRpU2hpdcXcuuSduvqkGo9zO41sovm0Xw_yT6_ef1p-a44O3-7Wp6eFZpyPBYUYAKpgSVkXFMGMUS05AQrJAmpCW0YxqxUJeNSSQB4CaqaK1WVECuOVV2eZE_33qHzUcx9iwIinowUUJCI1Z6ovdyIIdhehq3w0oqfBz60QobR6s4IAyChWLKGMoU5YCxZUjGAdaOoViS5Xs3VJtWbWhs3BtkdSA8jzq5F678JWHFGwE7wfBYE_3UycRS9jdp0nXTGT1FQgGAaJP8rCDnloMIogc_-AG9vwky1Mn2ndY1Pr6d3SnEKK0gJrFCVqMUtVLpqk0ad_ovGpvODhBcHCYkZzdXYyilGsfr44T_Y9__Onn85ZPGe1cHHGExzPQ4IxG6bfjVE7LZJzNuU0p7cHOXvpHl9yh-PLxln</recordid><startdate>20070101</startdate><enddate>20070101</enddate><creator>van der Pluijm, Ingrid</creator><creator>Garinis, George A</creator><creator>Brandt, Renata M C</creator><creator>Gorgels, Theo G M F</creator><creator>Wijnhoven, Susan W</creator><creator>Diderich, Karin E M</creator><creator>de Wit, Jan</creator><creator>Mitchell, James R</creator><creator>van Oostrom, Conny</creator><creator>Beems, Rudolf</creator><creator>Niedernhofer, Laura J</creator><creator>Velasco, Susana</creator><creator>Friedberg, Errol C</creator><creator>Tanaka, Kiyoji</creator><creator>van Steeg, Harry</creator><creator>Hoeijmakers, Jan H J</creator><creator>van der Horst, Gijsbertus T J</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISN</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</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>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PATMY</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><scope>CZG</scope></search><sort><creationdate>20070101</creationdate><title>Impaired genome maintenance suppresses the growth hormone--insulin-like growth factor 1 axis in mice with Cockayne syndrome</title><author>van der Pluijm, Ingrid ; Garinis, George A ; Brandt, Renata M C ; Gorgels, Theo G M F ; Wijnhoven, Susan W ; Diderich, Karin E M ; de Wit, Jan ; Mitchell, James R ; van Oostrom, Conny ; Beems, Rudolf ; Niedernhofer, Laura J ; Velasco, Susana ; Friedberg, Errol C ; Tanaka, Kiyoji ; van Steeg, Harry ; Hoeijmakers, Jan H J ; van der Horst, Gijsbertus T J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c794t-704517e13189c78141273954b2a55d57f84483b389aba009306d9bb6314b94bd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Age</topic><topic>Aging</topic><topic>Animals</topic><topic>Antioxidants - 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Here, complete inactivation of NER in Csb(m/m)/Xpa(-/-) mutants causes a phenotype that reliably mimics the human progeroid CS syndrome. Newborn Csb(m/m)/Xpa(-/-) mice display attenuated growth, progressive neurological dysfunction, retinal degeneration, cachexia, kyphosis, and die before weaning. Mouse liver transcriptome analysis and several physiological endpoints revealed systemic suppression of the growth hormone/insulin-like growth factor 1 (GH/IGF1) somatotroph axis and oxidative metabolism, increased antioxidant responses, and hypoglycemia together with hepatic glycogen and fat accumulation. Broad genome-wide parallels between Csb(m/m)/Xpa(-/-) and naturally aged mouse liver transcriptomes suggested that these changes are intrinsic to natural ageing and the DNA repair-deficient mice. Importantly, wild-type mice exposed to a low dose of chronic genotoxic stress recapitulated this response, thereby pointing to a novel link between genome instability and the age-related decline of the somatotroph axis.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>17326724</pmid><doi>10.1371/journal.pbio.0050002</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1291897070 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Age Aging Animals Antioxidants - pharmacology Cockayne syndrome Cockayne Syndrome - etiology Cockayne Syndrome - genetics Computational Biology Defects Deoxyribonucleic acid Diabetes and Endocrinology Diethylhexyl Phthalate - pharmacology DNA DNA damage DNA mismatch repair DNA Repair DNA Repair Enzymes - genetics DNA-Binding Proteins - genetics Experiments Fatty Acids - biosynthesis Genetic aspects Genetics and Genomics Genome - genetics Genomes Geriatrics Glucose - metabolism Growth Hormone - genetics Hypotheses Insulin-Like Growth Factor I - genetics Insulin-Like Growth Factor I - metabolism Insulin-like growth factors Liver - metabolism Male Mammals Mice Mice, Inbred C57BL Mice, Knockout Mus (Mouse) Oxidative stress Poly-ADP-Ribose Binding Proteins Proteins Radiation, Ionizing Rodents Somatotrophs - metabolism Xeroderma Pigmentosum Group A Protein - genetics |
| title | Impaired genome maintenance suppresses the growth hormone--insulin-like growth factor 1 axis in mice with Cockayne syndrome |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-03T09%3A24%3A22IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Impaired%20genome%20maintenance%20suppresses%20the%20growth%20hormone--insulin-like%20growth%20factor%201%20axis%20in%20mice%20with%20Cockayne%20syndrome&rft.jtitle=PLoS%20biology&rft.au=van%20der%20Pluijm,%20Ingrid&rft.date=2007-01-01&rft.volume=5&rft.issue=1&rft.spage=e2&rft.epage=e2&rft.pages=e2-e2&rft.issn=1545-7885&rft.eissn=1545-7885&rft_id=info:doi/10.1371/journal.pbio.0050002&rft_dat=%3Cgale_plos_%3EA161751626%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1291897070&rft_id=info:pmid/17326724&rft_galeid=A161751626&rft_doaj_id=oai_doaj_org_article_e01574a8f78b49088291bb604cfb7cb5&rfr_iscdi=true |