OPA1 increases the risk of normal but not high tension glaucoma
BackgroundPrimary open angle glaucoma is a progressive optic neuropathy characterised by the selective loss of retinal ganglion cells, pathological optic disc cupping and visual field defects. The OPA1 gene encodes an inner mitochondrial membrane protein crucial for normal mitochondrial function, an...
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| Veröffentlicht in: | Journal of medical genetics 2010-02, Vol.47 (2), p.120-125 |
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| creator | Yu-Wai-Man, P Stewart, J D Hudson, G Andrews, R M Griffiths, P G Birch, M K Chinnery, P F |
| description | BackgroundPrimary open angle glaucoma is a progressive optic neuropathy characterised by the selective loss of retinal ganglion cells, pathological optic disc cupping and visual field defects. The OPA1 gene encodes an inner mitochondrial membrane protein crucial for normal mitochondrial function, and pathogenic mutations cause autosomal dominant optic atrophy by specifically targeting retinal ganglion cells. This raises the distinct possibility that more subtle genetic variations in OPA1 could alter the risk of developing glaucoma.Methods137 patients with primary open angle glaucoma (67 patients with high-tension glaucoma (HTG), 70 patients with normal-tension glaucoma (NTG)) and 75 controls from the North East of England were studied. Three single-nucleotide polymorphisms in intron 8 (IVS8+4c→t and IVS8+32t→c) and exon 4 (c.473A→G) of the OPA1 gene were genotyped in the study group. In addition, the entire OPA1 coding region was sequenced in 24 individuals with the CT/TT compound genotype using standard BigDye chemistries.ResultsThere was no difference in either allele or genotype frequency for the IVS8+32t→c single-nucleotide polymorphisms between patients and controls, but there was a significant association between the T allele at IVS8+4c→t and the risk of developing NTG (OR=2.04, 95% CI=1.10 to 3.81, p=0.004), but not HTG. Logistic regression analysis also confirmed a strong association between the CT/TT compound genotype at IVS8+4 and IVS8+32 with NTG (OR=29.75, 95% CI=3.83 to 231.21, p=0.001).ConclusionsThe CT/TT compound genotype at IVS8+4 and IVS8+32 is a strong genetic risk determinant for NTG but not HTG. |
| doi_str_mv | 10.1136/jmg.2009.067512 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4038487</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>733950169</sourcerecordid><originalsourceid>FETCH-LOGICAL-b523t-bf986a1577c52040408f354d6d879e91f3c6bed2501d74433a45c541762eac283</originalsourceid><addsrcrecordid>eNqFkduL1DAYxYMo7uzqs29SEFkQOpsv974oy-h6YXAXvLyGNE1nMts2a9KK_vdm6DBeXiQPCXy_nO8cDkJPAC8BqLjY9ZslwbhaYiE5kHtoAUyoUhDG7qMFxoSUhFf0BJ2mtMMYqATxEJ1AxRUQyRbo1fXNJRR-sNGZ5FIxbl0RfbotQlsMIfamK-ppzM-x2PrNthjdkHwYik1nJht68wg9aE2X3OPDfYa-XL35vHpXrq_fvl9drsuaEzqWdVspYYBLaTnBLB_VUs4a0ShZuQpaakXtGsIxNJIxSg3jljOQgjhjiaJn6OWsezfVvWusG8ZoOn0XfW_iTx2M139PBr_Vm_BdM0wVUzILnB8EYvg2uTTq3ifrus4MLkxJS0qrvF1UmXz2D7kLUxxyOg1SAVRMwd7QxUzZGFKKrj16Aaz33ejcjd53o-du8o-nf0b4zR_KyMDzA2CSNV0bzWB9OnKEUKmU2EcpZ86n0f04zk281Xkquf74daVf80_rK_iw1jeZfzHzdb_7r8tfP4Sxig</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1781194818</pqid></control><display><type>article</type><title>OPA1 increases the risk of normal but not high tension glaucoma</title><source>MEDLINE</source><source>BMJ Journals - NESLi2</source><creator>Yu-Wai-Man, P ; Stewart, J D ; Hudson, G ; Andrews, R M ; Griffiths, P G ; Birch, M K ; Chinnery, P F</creator><creatorcontrib>Yu-Wai-Man, P ; Stewart, J D ; Hudson, G ; Andrews, R M ; Griffiths, P G ; Birch, M K ; Chinnery, P F</creatorcontrib><description>BackgroundPrimary open angle glaucoma is a progressive optic neuropathy characterised by the selective loss of retinal ganglion cells, pathological optic disc cupping and visual field defects. The OPA1 gene encodes an inner mitochondrial membrane protein crucial for normal mitochondrial function, and pathogenic mutations cause autosomal dominant optic atrophy by specifically targeting retinal ganglion cells. This raises the distinct possibility that more subtle genetic variations in OPA1 could alter the risk of developing glaucoma.Methods137 patients with primary open angle glaucoma (67 patients with high-tension glaucoma (HTG), 70 patients with normal-tension glaucoma (NTG)) and 75 controls from the North East of England were studied. Three single-nucleotide polymorphisms in intron 8 (IVS8+4c→t and IVS8+32t→c) and exon 4 (c.473A→G) of the OPA1 gene were genotyped in the study group. In addition, the entire OPA1 coding region was sequenced in 24 individuals with the CT/TT compound genotype using standard BigDye chemistries.ResultsThere was no difference in either allele or genotype frequency for the IVS8+32t→c single-nucleotide polymorphisms between patients and controls, but there was a significant association between the T allele at IVS8+4c→t and the risk of developing NTG (OR=2.04, 95% CI=1.10 to 3.81, p=0.004), but not HTG. Logistic regression analysis also confirmed a strong association between the CT/TT compound genotype at IVS8+4 and IVS8+32 with NTG (OR=29.75, 95% CI=3.83 to 231.21, p=0.001).ConclusionsThe CT/TT compound genotype at IVS8+4 and IVS8+32 is a strong genetic risk determinant for NTG but not HTG.</description><identifier>ISSN: 0022-2593</identifier><identifier>EISSN: 1468-6244</identifier><identifier>DOI: 10.1136/jmg.2009.067512</identifier><identifier>PMID: 19581274</identifier><identifier>CODEN: JMDGAE</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd</publisher><subject>Aged ; Aged, 80 and over ; Amino Acid Sequence ; Biological and medical sciences ; Case-Control Studies ; Chi-Square Distribution ; Dominant optic atrophy ; Fundamental and applied biological sciences. Psychology ; General aspects. Genetic counseling ; Genetic Predisposition to Disease ; Genetics of eukaryotes. Biological and molecular evolution ; Genotype ; Glaucoma ; Glaucoma and intraocular pressure ; Glaucoma, Open-Angle - genetics ; GTP Phosphohydrolases - genetics ; Haplotypes ; Humans ; Introns ; Logistic Models ; Medical genetics ; Medical sciences ; mitochondria ; Molecular and cellular biology ; molecular genetics ; Molecular Sequence Data ; neuroophthalmology ; OPA1 ; Ophthalmology ; optic nerve ; Polymorphism, Single Nucleotide ; Sequence Alignment</subject><ispartof>Journal of medical genetics, 2010-02, Vol.47 (2), p.120-125</ispartof><rights>2009, Published by the BMJ Publishing Group Limited For permission to use, (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright: 2009 (c) 2009, Published by the BMJ Publishing Group Limited For permission to use, (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b523t-bf986a1577c52040408f354d6d879e91f3c6bed2501d74433a45c541762eac283</citedby><cites>FETCH-LOGICAL-b523t-bf986a1577c52040408f354d6d879e91f3c6bed2501d74433a45c541762eac283</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://jmg.bmj.com/content/47/2/120.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttps://jmg.bmj.com/content/47/2/120.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,230,314,776,780,881,3183,23550,27901,27902,77343,77374</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22378867$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19581274$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yu-Wai-Man, P</creatorcontrib><creatorcontrib>Stewart, J D</creatorcontrib><creatorcontrib>Hudson, G</creatorcontrib><creatorcontrib>Andrews, R M</creatorcontrib><creatorcontrib>Griffiths, P G</creatorcontrib><creatorcontrib>Birch, M K</creatorcontrib><creatorcontrib>Chinnery, P F</creatorcontrib><title>OPA1 increases the risk of normal but not high tension glaucoma</title><title>Journal of medical genetics</title><addtitle>J Med Genet</addtitle><description>BackgroundPrimary open angle glaucoma is a progressive optic neuropathy characterised by the selective loss of retinal ganglion cells, pathological optic disc cupping and visual field defects. The OPA1 gene encodes an inner mitochondrial membrane protein crucial for normal mitochondrial function, and pathogenic mutations cause autosomal dominant optic atrophy by specifically targeting retinal ganglion cells. This raises the distinct possibility that more subtle genetic variations in OPA1 could alter the risk of developing glaucoma.Methods137 patients with primary open angle glaucoma (67 patients with high-tension glaucoma (HTG), 70 patients with normal-tension glaucoma (NTG)) and 75 controls from the North East of England were studied. Three single-nucleotide polymorphisms in intron 8 (IVS8+4c→t and IVS8+32t→c) and exon 4 (c.473A→G) of the OPA1 gene were genotyped in the study group. In addition, the entire OPA1 coding region was sequenced in 24 individuals with the CT/TT compound genotype using standard BigDye chemistries.ResultsThere was no difference in either allele or genotype frequency for the IVS8+32t→c single-nucleotide polymorphisms between patients and controls, but there was a significant association between the T allele at IVS8+4c→t and the risk of developing NTG (OR=2.04, 95% CI=1.10 to 3.81, p=0.004), but not HTG. Logistic regression analysis also confirmed a strong association between the CT/TT compound genotype at IVS8+4 and IVS8+32 with NTG (OR=29.75, 95% CI=3.83 to 231.21, p=0.001).ConclusionsThe CT/TT compound genotype at IVS8+4 and IVS8+32 is a strong genetic risk determinant for NTG but not HTG.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Amino Acid Sequence</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>Chi-Square Distribution</subject><subject>Dominant optic atrophy</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>General aspects. Genetic counseling</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetics of eukaryotes. Biological and molecular evolution</subject><subject>Genotype</subject><subject>Glaucoma</subject><subject>Glaucoma and intraocular pressure</subject><subject>Glaucoma, Open-Angle - genetics</subject><subject>GTP Phosphohydrolases - genetics</subject><subject>Haplotypes</subject><subject>Humans</subject><subject>Introns</subject><subject>Logistic Models</subject><subject>Medical genetics</subject><subject>Medical sciences</subject><subject>mitochondria</subject><subject>Molecular and cellular biology</subject><subject>molecular genetics</subject><subject>Molecular Sequence Data</subject><subject>neuroophthalmology</subject><subject>OPA1</subject><subject>Ophthalmology</subject><subject>optic nerve</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Sequence Alignment</subject><issn>0022-2593</issn><issn>1468-6244</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkduL1DAYxYMo7uzqs29SEFkQOpsv974oy-h6YXAXvLyGNE1nMts2a9KK_vdm6DBeXiQPCXy_nO8cDkJPAC8BqLjY9ZslwbhaYiE5kHtoAUyoUhDG7qMFxoSUhFf0BJ2mtMMYqATxEJ1AxRUQyRbo1fXNJRR-sNGZ5FIxbl0RfbotQlsMIfamK-ppzM-x2PrNthjdkHwYik1nJht68wg9aE2X3OPDfYa-XL35vHpXrq_fvl9drsuaEzqWdVspYYBLaTnBLB_VUs4a0ShZuQpaakXtGsIxNJIxSg3jljOQgjhjiaJn6OWsezfVvWusG8ZoOn0XfW_iTx2M139PBr_Vm_BdM0wVUzILnB8EYvg2uTTq3ifrus4MLkxJS0qrvF1UmXz2D7kLUxxyOg1SAVRMwd7QxUzZGFKKrj16Aaz33ejcjd53o-du8o-nf0b4zR_KyMDzA2CSNV0bzWB9OnKEUKmU2EcpZ86n0f04zk281Xkquf74daVf80_rK_iw1jeZfzHzdb_7r8tfP4Sxig</recordid><startdate>20100201</startdate><enddate>20100201</enddate><creator>Yu-Wai-Man, P</creator><creator>Stewart, J D</creator><creator>Hudson, G</creator><creator>Andrews, R M</creator><creator>Griffiths, P G</creator><creator>Birch, M K</creator><creator>Chinnery, P F</creator><general>BMJ Publishing Group Ltd</general><general>BMJ Publishing Group</general><general>BMJ Publishing Group LTD</general><scope>BSCLL</scope><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>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AF</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>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</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>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20100201</creationdate><title>OPA1 increases the risk of normal but not high tension glaucoma</title><author>Yu-Wai-Man, P ; Stewart, J D ; Hudson, G ; Andrews, R M ; Griffiths, P G ; Birch, M K ; Chinnery, P F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b523t-bf986a1577c52040408f354d6d879e91f3c6bed2501d74433a45c541762eac283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Amino Acid Sequence</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>Chi-Square Distribution</topic><topic>Dominant optic atrophy</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>General aspects. Genetic counseling</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetics of eukaryotes. Biological and molecular evolution</topic><topic>Genotype</topic><topic>Glaucoma</topic><topic>Glaucoma and intraocular pressure</topic><topic>Glaucoma, Open-Angle - genetics</topic><topic>GTP Phosphohydrolases - genetics</topic><topic>Haplotypes</topic><topic>Humans</topic><topic>Introns</topic><topic>Logistic Models</topic><topic>Medical genetics</topic><topic>Medical sciences</topic><topic>mitochondria</topic><topic>Molecular and cellular biology</topic><topic>molecular genetics</topic><topic>Molecular Sequence Data</topic><topic>neuroophthalmology</topic><topic>OPA1</topic><topic>Ophthalmology</topic><topic>optic nerve</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Sequence Alignment</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yu-Wai-Man, P</creatorcontrib><creatorcontrib>Stewart, J D</creatorcontrib><creatorcontrib>Hudson, G</creatorcontrib><creatorcontrib>Andrews, R M</creatorcontrib><creatorcontrib>Griffiths, P G</creatorcontrib><creatorcontrib>Birch, M K</creatorcontrib><creatorcontrib>Chinnery, P F</creatorcontrib><collection>Istex</collection><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>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>Science Database (Alumni Edition)</collection><collection>STEM 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>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>Science Database</collection><collection>Biological Science Database</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of medical genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yu-Wai-Man, P</au><au>Stewart, J D</au><au>Hudson, G</au><au>Andrews, R M</au><au>Griffiths, P G</au><au>Birch, M K</au><au>Chinnery, P F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>OPA1 increases the risk of normal but not high tension glaucoma</atitle><jtitle>Journal of medical genetics</jtitle><addtitle>J Med Genet</addtitle><date>2010-02-01</date><risdate>2010</risdate><volume>47</volume><issue>2</issue><spage>120</spage><epage>125</epage><pages>120-125</pages><issn>0022-2593</issn><eissn>1468-6244</eissn><coden>JMDGAE</coden><abstract>BackgroundPrimary open angle glaucoma is a progressive optic neuropathy characterised by the selective loss of retinal ganglion cells, pathological optic disc cupping and visual field defects. The OPA1 gene encodes an inner mitochondrial membrane protein crucial for normal mitochondrial function, and pathogenic mutations cause autosomal dominant optic atrophy by specifically targeting retinal ganglion cells. This raises the distinct possibility that more subtle genetic variations in OPA1 could alter the risk of developing glaucoma.Methods137 patients with primary open angle glaucoma (67 patients with high-tension glaucoma (HTG), 70 patients with normal-tension glaucoma (NTG)) and 75 controls from the North East of England were studied. Three single-nucleotide polymorphisms in intron 8 (IVS8+4c→t and IVS8+32t→c) and exon 4 (c.473A→G) of the OPA1 gene were genotyped in the study group. In addition, the entire OPA1 coding region was sequenced in 24 individuals with the CT/TT compound genotype using standard BigDye chemistries.ResultsThere was no difference in either allele or genotype frequency for the IVS8+32t→c single-nucleotide polymorphisms between patients and controls, but there was a significant association between the T allele at IVS8+4c→t and the risk of developing NTG (OR=2.04, 95% CI=1.10 to 3.81, p=0.004), but not HTG. Logistic regression analysis also confirmed a strong association between the CT/TT compound genotype at IVS8+4 and IVS8+32 with NTG (OR=29.75, 95% CI=3.83 to 231.21, p=0.001).ConclusionsThe CT/TT compound genotype at IVS8+4 and IVS8+32 is a strong genetic risk determinant for NTG but not HTG.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd</pub><pmid>19581274</pmid><doi>10.1136/jmg.2009.067512</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Aged, 80 and over Amino Acid Sequence Biological and medical sciences Case-Control Studies Chi-Square Distribution Dominant optic atrophy Fundamental and applied biological sciences. Psychology General aspects. Genetic counseling Genetic Predisposition to Disease Genetics of eukaryotes. Biological and molecular evolution Genotype Glaucoma Glaucoma and intraocular pressure Glaucoma, Open-Angle - genetics GTP Phosphohydrolases - genetics Haplotypes Humans Introns Logistic Models Medical genetics Medical sciences mitochondria Molecular and cellular biology molecular genetics Molecular Sequence Data neuroophthalmology OPA1 Ophthalmology optic nerve Polymorphism, Single Nucleotide Sequence Alignment |
| title | OPA1 increases the risk of normal but not high tension glaucoma |
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