A Genetic Variant in GPR126 Causing a Decreased Inclusion of Exon 6 Is Associated with Cartilage Development in Adolescent Idiopathic Scoliosis Population
Adolescent idiopathic scoliosis (AIS) is the most common spinal deformity disease in adolescents but its etiology and pathogenesis are still unclear. The current study aims to identify the relationship between single nucleotide polymorphisms (SNPs) of G protein-coupled receptor 126 (GPR126) gene and...
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| creator | Gao, Rui Lin, Tao Jiang, Heng Shao, Wei Xu, Enjie Zhou, Xuhui |
| description | Adolescent idiopathic scoliosis (AIS) is the most common spinal deformity disease in adolescents but its etiology and pathogenesis are still unclear. The current study aims to identify the relationship between single nucleotide polymorphisms (SNPs) of G protein-coupled receptor 126 (GPR126) gene and AIS predisposition. GPR126 contains 26 exons and alternative splicing of exon 6 and exon 25 produces 4 protein-coding transcripts. We genotyped SNPs of GPR126 gene around exon 6 and exon 25 in 131 Chinese AIS patients and 132 healthy controls and provided evidence that SNP rs41289839 G>A is strongly associated with AIS susceptibility. Linkage disequilibrium analysis suggests that rs41289839 and other AIS-related SNPs were in strong LD. Next, we demonstrated that rs41289839 G>A inhibits the inclusion of exon 6 during alternative splicing, resulting in a decreased expression level of exon 6-included transcript (GPR126-exon6in) relative to the exon 6 excluded transcript (GPR126-exon6ex) by minigene assay. Chondrogenic differentiation experiment showed that GPR126-exon6in has a high expression level relative to GPR126-exon6ex during chondrogenic differentiation of hMSCs. Our findings indicate that newly discovered SNP is related to cartilage development and may provide valuable insights into the etiology and pathogenesis of adolescent idiopathic scoliosis. |
| doi_str_mv | 10.1155/2019/4678969 |
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The current study aims to identify the relationship between single nucleotide polymorphisms (SNPs) of G protein-coupled receptor 126 (GPR126) gene and AIS predisposition. GPR126 contains 26 exons and alternative splicing of exon 6 and exon 25 produces 4 protein-coding transcripts. We genotyped SNPs of GPR126 gene around exon 6 and exon 25 in 131 Chinese AIS patients and 132 healthy controls and provided evidence that SNP rs41289839 G>A is strongly associated with AIS susceptibility. Linkage disequilibrium analysis suggests that rs41289839 and other AIS-related SNPs were in strong LD. Next, we demonstrated that rs41289839 G>A inhibits the inclusion of exon 6 during alternative splicing, resulting in a decreased expression level of exon 6-included transcript (GPR126-exon6in) relative to the exon 6 excluded transcript (GPR126-exon6ex) by minigene assay. Chondrogenic differentiation experiment showed that GPR126-exon6in has a high expression level relative to GPR126-exon6ex during chondrogenic differentiation of hMSCs. Our findings indicate that newly discovered SNP is related to cartilage development and may provide valuable insights into the etiology and pathogenesis of adolescent idiopathic scoliosis.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2019/4678969</identifier><identifier>PMID: 30886859</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Adolescents ; Alternative splicing ; Cartilage ; Deformation mechanisms ; Deoxyribonucleic acid ; Differentiation ; DNA ; Etiology ; Exons ; Genetic diversity ; Genetic variance ; Genetics ; Linkage analysis ; Linkage disequilibrium ; Metabolism ; Pathogenesis ; Patients ; Polymorphism ; Proteins ; Scoliosis ; Single-nucleotide polymorphism ; Studies ; Transcription</subject><ispartof>BioMed research international, 2019-01, Vol.2019 (2019), p.1-8</ispartof><rights>Copyright © 2019 Enjie Xu et al.</rights><rights>Copyright © 2019 Enjie Xu et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2019 Enjie Xu et al. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-63b8e50aba64f7affe0d1d488b2951a0987b77e1c80bbae2c8382dd2b860ec123</citedby><cites>FETCH-LOGICAL-c471t-63b8e50aba64f7affe0d1d488b2951a0987b77e1c80bbae2c8382dd2b860ec123</cites><orcidid>0000-0002-8026-5468 ; 0000-0003-0695-7180</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/PMC6388357/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6388357/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30886859$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Gallone, Salvatore</contributor><contributor>Salvatore Gallone</contributor><creatorcontrib>Gao, Rui</creatorcontrib><creatorcontrib>Lin, Tao</creatorcontrib><creatorcontrib>Jiang, Heng</creatorcontrib><creatorcontrib>Shao, Wei</creatorcontrib><creatorcontrib>Xu, Enjie</creatorcontrib><creatorcontrib>Zhou, Xuhui</creatorcontrib><title>A Genetic Variant in GPR126 Causing a Decreased Inclusion of Exon 6 Is Associated with Cartilage Development in Adolescent Idiopathic Scoliosis Population</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>Adolescent idiopathic scoliosis (AIS) is the most common spinal deformity disease in adolescents but its etiology and pathogenesis are still unclear. The current study aims to identify the relationship between single nucleotide polymorphisms (SNPs) of G protein-coupled receptor 126 (GPR126) gene and AIS predisposition. GPR126 contains 26 exons and alternative splicing of exon 6 and exon 25 produces 4 protein-coding transcripts. We genotyped SNPs of GPR126 gene around exon 6 and exon 25 in 131 Chinese AIS patients and 132 healthy controls and provided evidence that SNP rs41289839 G>A is strongly associated with AIS susceptibility. Linkage disequilibrium analysis suggests that rs41289839 and other AIS-related SNPs were in strong LD. Next, we demonstrated that rs41289839 G>A inhibits the inclusion of exon 6 during alternative splicing, resulting in a decreased expression level of exon 6-included transcript (GPR126-exon6in) relative to the exon 6 excluded transcript (GPR126-exon6ex) by minigene assay. Chondrogenic differentiation experiment showed that GPR126-exon6in has a high expression level relative to GPR126-exon6ex during chondrogenic differentiation of hMSCs. Our findings indicate that newly discovered SNP is related to cartilage development and may provide valuable insights into the etiology and pathogenesis of adolescent idiopathic scoliosis.</description><subject>Adolescents</subject><subject>Alternative splicing</subject><subject>Cartilage</subject><subject>Deformation mechanisms</subject><subject>Deoxyribonucleic acid</subject><subject>Differentiation</subject><subject>DNA</subject><subject>Etiology</subject><subject>Exons</subject><subject>Genetic diversity</subject><subject>Genetic variance</subject><subject>Genetics</subject><subject>Linkage analysis</subject><subject>Linkage disequilibrium</subject><subject>Metabolism</subject><subject>Pathogenesis</subject><subject>Patients</subject><subject>Polymorphism</subject><subject>Proteins</subject><subject>Scoliosis</subject><subject>Single-nucleotide polymorphism</subject><subject>Studies</subject><subject>Transcription</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkU1vEzEQhlcIRKvSG2dkiQsShNrrtde-IEWhhEiVqPi6rma9s4krx07t3Rb-Cr8WrxLCxwlfxmM_886M3qJ4yuhrxoS4KCnTF5WslZb6QXFaclbNJKvYw-Od85PiPKUbmo9ikmr5uDjhVCmphD4tfszJEj0O1pCvEC34gVhPltcfWSnJAsZk_ZoAeYsmIiTsyMobl1-DJ6Enl99ylGSVyDylYCwMmbi3wyaXxsE6WGMuvUMXdlvcS8-74DCZKVt1Nuxg2OTen0xwNiSbyHXYjQ6G3OBJ8agHl_D8EM-KL-8uPy_ez64-LFeL-dXMVDUbZpK3CgWFFmTV19D3SDvWVUq1pRYMqFZ1W9fIjKJtC1gaxVXZdWWrJEXDSn5WvNnr7sZ2i900WgTX7KLdQvzeBLDN3z_ebpp1uGskV4qLOgu8OAjEcDtiGpqtzRs6Bx7DmJqS6YpxXekJff4PehPG6PN6mVJCqJrqKlOv9pSJIaWI_XEYRpvJ92byvTn4nvFnfy5whH-5nIGXe2BjfQf39j_lMDPYw2-alUIwwX8CjmzAZg</recordid><startdate>20190101</startdate><enddate>20190101</enddate><creator>Gao, Rui</creator><creator>Lin, Tao</creator><creator>Jiang, Heng</creator><creator>Shao, Wei</creator><creator>Xu, Enjie</creator><creator>Zhou, Xuhui</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</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>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-8026-5468</orcidid><orcidid>https://orcid.org/0000-0003-0695-7180</orcidid></search><sort><creationdate>20190101</creationdate><title>A Genetic Variant in GPR126 Causing a Decreased Inclusion of Exon 6 Is Associated with Cartilage Development in Adolescent Idiopathic Scoliosis Population</title><author>Gao, Rui ; Lin, Tao ; Jiang, Heng ; Shao, Wei ; Xu, Enjie ; Zhou, Xuhui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c471t-63b8e50aba64f7affe0d1d488b2951a0987b77e1c80bbae2c8382dd2b860ec123</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adolescents</topic><topic>Alternative splicing</topic><topic>Cartilage</topic><topic>Deformation mechanisms</topic><topic>Deoxyribonucleic acid</topic><topic>Differentiation</topic><topic>DNA</topic><topic>Etiology</topic><topic>Exons</topic><topic>Genetic diversity</topic><topic>Genetic variance</topic><topic>Genetics</topic><topic>Linkage analysis</topic><topic>Linkage disequilibrium</topic><topic>Metabolism</topic><topic>Pathogenesis</topic><topic>Patients</topic><topic>Polymorphism</topic><topic>Proteins</topic><topic>Scoliosis</topic><topic>Single-nucleotide polymorphism</topic><topic>Studies</topic><topic>Transcription</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gao, Rui</creatorcontrib><creatorcontrib>Lin, Tao</creatorcontrib><creatorcontrib>Jiang, Heng</creatorcontrib><creatorcontrib>Shao, Wei</creatorcontrib><creatorcontrib>Xu, Enjie</creatorcontrib><creatorcontrib>Zhou, Xuhui</creatorcontrib><collection>الدوريات العلمية والإحصائية - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gao, Rui</au><au>Lin, Tao</au><au>Jiang, Heng</au><au>Shao, Wei</au><au>Xu, Enjie</au><au>Zhou, Xuhui</au><au>Gallone, Salvatore</au><au>Salvatore Gallone</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Genetic Variant in GPR126 Causing a Decreased Inclusion of Exon 6 Is Associated with Cartilage Development in Adolescent Idiopathic Scoliosis Population</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2019-01-01</date><risdate>2019</risdate><volume>2019</volume><issue>2019</issue><spage>1</spage><epage>8</epage><pages>1-8</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Adolescent idiopathic scoliosis (AIS) is the most common spinal deformity disease in adolescents but its etiology and pathogenesis are still unclear. The current study aims to identify the relationship between single nucleotide polymorphisms (SNPs) of G protein-coupled receptor 126 (GPR126) gene and AIS predisposition. GPR126 contains 26 exons and alternative splicing of exon 6 and exon 25 produces 4 protein-coding transcripts. We genotyped SNPs of GPR126 gene around exon 6 and exon 25 in 131 Chinese AIS patients and 132 healthy controls and provided evidence that SNP rs41289839 G>A is strongly associated with AIS susceptibility. Linkage disequilibrium analysis suggests that rs41289839 and other AIS-related SNPs were in strong LD. Next, we demonstrated that rs41289839 G>A inhibits the inclusion of exon 6 during alternative splicing, resulting in a decreased expression level of exon 6-included transcript (GPR126-exon6in) relative to the exon 6 excluded transcript (GPR126-exon6ex) by minigene assay. Chondrogenic differentiation experiment showed that GPR126-exon6in has a high expression level relative to GPR126-exon6ex during chondrogenic differentiation of hMSCs. Our findings indicate that newly discovered SNP is related to cartilage development and may provide valuable insights into the etiology and pathogenesis of adolescent idiopathic scoliosis.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>30886859</pmid><doi>10.1155/2019/4678969</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-8026-5468</orcidid><orcidid>https://orcid.org/0000-0003-0695-7180</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adolescents Alternative splicing Cartilage Deformation mechanisms Deoxyribonucleic acid Differentiation DNA Etiology Exons Genetic diversity Genetic variance Genetics Linkage analysis Linkage disequilibrium Metabolism Pathogenesis Patients Polymorphism Proteins Scoliosis Single-nucleotide polymorphism Studies Transcription |
| title | A Genetic Variant in GPR126 Causing a Decreased Inclusion of Exon 6 Is Associated with Cartilage Development in Adolescent Idiopathic Scoliosis Population |
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