Monocarboxylate Transporter 10 Functions as a Thyroid Hormone Transporter in Chondrocytes
Thyroid hormone is essential for normal proliferation and differentiation of chondrocytes. Thus, untreated congenital hypothyroidism is marked by severe short stature. The monocarboxylate transporter 8 (MCT8) is a highly specific transporter for thyroid hormone. The hallmarks of Allan-Herndon-Dudley...
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| Veröffentlicht in: | Endocrinology (Philadelphia) 2012-08, Vol.153 (8), p.4049-4058 |
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| creator | Abe, Sanae Namba, Noriyuki Abe, Makoto Fujiwara, Makoto Aikawa, Tomonao Kogo, Mikihiko Ozono, Keiichi |
| description | Thyroid hormone is essential for normal proliferation and differentiation of chondrocytes. Thus, untreated congenital hypothyroidism is marked by severe short stature. The monocarboxylate transporter 8 (MCT8) is a highly specific transporter for thyroid hormone. The hallmarks of Allan-Herndon-Dudley syndrome, caused by MCT8 mutations, are severe psychomotor retardation and elevated T3 levels. However, growth is mostly normal. We therefore hypothesized that growth plate chondrocytes use transporters other than MCT8 for thyroid hormone uptake. Extensive analysis of thyroid hormone transporter mRNA expression in mouse chondrogenic ATDC5 cells revealed that monocarboxylate transporter 10 (Mct10) was most abundantly expressed among the transporters known to be highly specific for thyroid hormone, namely Mct8, Mct10, and organic anion transporter 1c1. Expression levels of Mct10 mRNA diminished with chondrocyte differentiation in these cells. Accordingly, Mct10 mRNA was expressed most abundantly in the growth plate resting zone chondrocytes in vivo. Small interfering RNA-mediated knockdown of Mct10 mRNA in ATDC5 cells decreased [125I]T3 uptake up to 44% compared with negative control (P < 0.05). Moreover, silencing Mct10 mRNA expression abolished the known effects of T3, i.e. suppression of proliferation and enhancement of differentiation, in ATDC5 cells. These results suggest that Mct10 functions as a thyroid hormone transporter in chondrocytes and can explain at least in part why Allan-Herndon-Dudley syndrome patients do not exhibit significant growth impairment. |
| doi_str_mv | 10.1210/en.2011-1713 |
| format | Article |
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Thus, untreated congenital hypothyroidism is marked by severe short stature. The monocarboxylate transporter 8 (MCT8) is a highly specific transporter for thyroid hormone. The hallmarks of Allan-Herndon-Dudley syndrome, caused by MCT8 mutations, are severe psychomotor retardation and elevated T3 levels. However, growth is mostly normal. We therefore hypothesized that growth plate chondrocytes use transporters other than MCT8 for thyroid hormone uptake. Extensive analysis of thyroid hormone transporter mRNA expression in mouse chondrogenic ATDC5 cells revealed that monocarboxylate transporter 10 (Mct10) was most abundantly expressed among the transporters known to be highly specific for thyroid hormone, namely Mct8, Mct10, and organic anion transporter 1c1. Expression levels of Mct10 mRNA diminished with chondrocyte differentiation in these cells. Accordingly, Mct10 mRNA was expressed most abundantly in the growth plate resting zone chondrocytes in vivo. Small interfering RNA-mediated knockdown of Mct10 mRNA in ATDC5 cells decreased [125I]T3 uptake up to 44% compared with negative control (P < 0.05). Moreover, silencing Mct10 mRNA expression abolished the known effects of T3, i.e. suppression of proliferation and enhancement of differentiation, in ATDC5 cells. These results suggest that Mct10 functions as a thyroid hormone transporter in chondrocytes and can explain at least in part why Allan-Herndon-Dudley syndrome patients do not exhibit significant growth impairment.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2011-1713</identifier><identifier>PMID: 22719050</identifier><identifier>CODEN: ENDOAO</identifier><language>eng</language><publisher>Chevy Chase, MD: Endocrine Society</publisher><subject>Animals ; Biological and medical sciences ; Cell differentiation ; Cell Line ; Cell Proliferation ; Chondrocytes ; Chondrocytes - cytology ; Chondrocytes - metabolism ; Chondrogenesis ; Differentiation ; Fundamental and applied biological sciences. Psychology ; Gene expression ; Growth plate ; Hypothyroidism ; In Situ Hybridization ; Intellectual disabilities ; Membrane Transport Proteins - genetics ; Membrane Transport Proteins - metabolism ; Mice ; Mice, Inbred C57BL ; Monocarboxylic Acid Transporters - genetics ; Monocarboxylic Acid Transporters - metabolism ; RNA, Small Interfering ; siRNA ; Thyroid ; Thyroid gland ; Thyroid Hormones - metabolism ; Triiodothyronine ; Vertebrates: endocrinology</subject><ispartof>Endocrinology (Philadelphia), 2012-08, Vol.153 (8), p.4049-4058</ispartof><rights>Copyright © 2012 by The Endocrine Society</rights><rights>Copyright © 2012 by The Endocrine Society 2012</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c562t-2083fd5a8b0ed372395d7e9bd54fe784675fa8ae6924cbcdef863b4314fa83c83</citedby><cites>FETCH-LOGICAL-c562t-2083fd5a8b0ed372395d7e9bd54fe784675fa8ae6924cbcdef863b4314fa83c83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26161225$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22719050$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Abe, Sanae</creatorcontrib><creatorcontrib>Namba, Noriyuki</creatorcontrib><creatorcontrib>Abe, Makoto</creatorcontrib><creatorcontrib>Fujiwara, Makoto</creatorcontrib><creatorcontrib>Aikawa, Tomonao</creatorcontrib><creatorcontrib>Kogo, Mikihiko</creatorcontrib><creatorcontrib>Ozono, Keiichi</creatorcontrib><title>Monocarboxylate Transporter 10 Functions as a Thyroid Hormone Transporter in Chondrocytes</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>Thyroid hormone is essential for normal proliferation and differentiation of chondrocytes. Thus, untreated congenital hypothyroidism is marked by severe short stature. The monocarboxylate transporter 8 (MCT8) is a highly specific transporter for thyroid hormone. The hallmarks of Allan-Herndon-Dudley syndrome, caused by MCT8 mutations, are severe psychomotor retardation and elevated T3 levels. However, growth is mostly normal. We therefore hypothesized that growth plate chondrocytes use transporters other than MCT8 for thyroid hormone uptake. Extensive analysis of thyroid hormone transporter mRNA expression in mouse chondrogenic ATDC5 cells revealed that monocarboxylate transporter 10 (Mct10) was most abundantly expressed among the transporters known to be highly specific for thyroid hormone, namely Mct8, Mct10, and organic anion transporter 1c1. Expression levels of Mct10 mRNA diminished with chondrocyte differentiation in these cells. Accordingly, Mct10 mRNA was expressed most abundantly in the growth plate resting zone chondrocytes in vivo. Small interfering RNA-mediated knockdown of Mct10 mRNA in ATDC5 cells decreased [125I]T3 uptake up to 44% compared with negative control (P < 0.05). Moreover, silencing Mct10 mRNA expression abolished the known effects of T3, i.e. suppression of proliferation and enhancement of differentiation, in ATDC5 cells. These results suggest that Mct10 functions as a thyroid hormone transporter in chondrocytes and can explain at least in part why Allan-Herndon-Dudley syndrome patients do not exhibit significant growth impairment.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell differentiation</subject><subject>Cell Line</subject><subject>Cell Proliferation</subject><subject>Chondrocytes</subject><subject>Chondrocytes - cytology</subject><subject>Chondrocytes - metabolism</subject><subject>Chondrogenesis</subject><subject>Differentiation</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene expression</subject><subject>Growth plate</subject><subject>Hypothyroidism</subject><subject>In Situ Hybridization</subject><subject>Intellectual disabilities</subject><subject>Membrane Transport Proteins - genetics</subject><subject>Membrane Transport Proteins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Monocarboxylic Acid Transporters - genetics</subject><subject>Monocarboxylic Acid Transporters - metabolism</subject><subject>RNA, Small Interfering</subject><subject>siRNA</subject><subject>Thyroid</subject><subject>Thyroid gland</subject><subject>Thyroid Hormones - metabolism</subject><subject>Triiodothyronine</subject><subject>Vertebrates: endocrinology</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0Utr3DAQAGBRWpJtmlvOwVBKc4hTjR6WfCxL0wQSctkeejKyNCYOXsmVbOj--2qz24aUlMKA0PAxo9EQcgL0AhjQT-gvGAUoQQF_RRZQC1kqUPQ1WVAKvFSMqUPyNqWHfBVC8ANymFNQU0kX5Ptt8MGa2Iafm8FMWKyi8WkMccJYAC0uZ2-nPvhUmBzF6n4TQ--KqxDXwT_XvS-W98G7GOxmwvSOvOnMkPB4fx6Rb5dfVsur8ubu6_Xy801pZcWmklHNOyeNbik6rhivpVNYt06KDpUWlZKd0QarmgnbWoedrngrOIic5lbzI3K2qzvG8GPGNDXrPlkcBuMxzKmBCnJUWsP_KWWqUrUUKtP3f9GHMEefB2k4cFox0I_qfKdsDClF7Jox9msTN7lUs91Og77ZbqfZbifz033RuV2j-4N_ryODD3tgkjVDl3_X9unJ5TmAMZndx50L8_ivluW-Jd9J9C7Y2HscI6b0NM2LD_0FM9ezXQ</recordid><startdate>20120801</startdate><enddate>20120801</enddate><creator>Abe, Sanae</creator><creator>Namba, Noriyuki</creator><creator>Abe, Makoto</creator><creator>Fujiwara, Makoto</creator><creator>Aikawa, Tomonao</creator><creator>Kogo, Mikihiko</creator><creator>Ozono, Keiichi</creator><general>Endocrine Society</general><general>Oxford University Press</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>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20120801</creationdate><title>Monocarboxylate Transporter 10 Functions as a Thyroid Hormone Transporter in Chondrocytes</title><author>Abe, Sanae ; Namba, Noriyuki ; Abe, Makoto ; Fujiwara, Makoto ; Aikawa, Tomonao ; Kogo, Mikihiko ; Ozono, Keiichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c562t-2083fd5a8b0ed372395d7e9bd54fe784675fa8ae6924cbcdef863b4314fa83c83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell differentiation</topic><topic>Cell Line</topic><topic>Cell Proliferation</topic><topic>Chondrocytes</topic><topic>Chondrocytes - cytology</topic><topic>Chondrocytes - metabolism</topic><topic>Chondrogenesis</topic><topic>Differentiation</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene expression</topic><topic>Growth plate</topic><topic>Hypothyroidism</topic><topic>In Situ Hybridization</topic><topic>Intellectual disabilities</topic><topic>Membrane Transport Proteins - genetics</topic><topic>Membrane Transport Proteins - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Monocarboxylic Acid Transporters - genetics</topic><topic>Monocarboxylic Acid Transporters - metabolism</topic><topic>RNA, Small Interfering</topic><topic>siRNA</topic><topic>Thyroid</topic><topic>Thyroid gland</topic><topic>Thyroid Hormones - metabolism</topic><topic>Triiodothyronine</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Abe, Sanae</creatorcontrib><creatorcontrib>Namba, Noriyuki</creatorcontrib><creatorcontrib>Abe, Makoto</creatorcontrib><creatorcontrib>Fujiwara, Makoto</creatorcontrib><creatorcontrib>Aikawa, Tomonao</creatorcontrib><creatorcontrib>Kogo, Mikihiko</creatorcontrib><creatorcontrib>Ozono, Keiichi</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>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Endocrinology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Abe, Sanae</au><au>Namba, Noriyuki</au><au>Abe, Makoto</au><au>Fujiwara, Makoto</au><au>Aikawa, Tomonao</au><au>Kogo, Mikihiko</au><au>Ozono, Keiichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Monocarboxylate Transporter 10 Functions as a Thyroid Hormone Transporter in Chondrocytes</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2012-08-01</date><risdate>2012</risdate><volume>153</volume><issue>8</issue><spage>4049</spage><epage>4058</epage><pages>4049-4058</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><coden>ENDOAO</coden><abstract>Thyroid hormone is essential for normal proliferation and differentiation of chondrocytes. Thus, untreated congenital hypothyroidism is marked by severe short stature. The monocarboxylate transporter 8 (MCT8) is a highly specific transporter for thyroid hormone. The hallmarks of Allan-Herndon-Dudley syndrome, caused by MCT8 mutations, are severe psychomotor retardation and elevated T3 levels. However, growth is mostly normal. We therefore hypothesized that growth plate chondrocytes use transporters other than MCT8 for thyroid hormone uptake. Extensive analysis of thyroid hormone transporter mRNA expression in mouse chondrogenic ATDC5 cells revealed that monocarboxylate transporter 10 (Mct10) was most abundantly expressed among the transporters known to be highly specific for thyroid hormone, namely Mct8, Mct10, and organic anion transporter 1c1. Expression levels of Mct10 mRNA diminished with chondrocyte differentiation in these cells. Accordingly, Mct10 mRNA was expressed most abundantly in the growth plate resting zone chondrocytes in vivo. Small interfering RNA-mediated knockdown of Mct10 mRNA in ATDC5 cells decreased [125I]T3 uptake up to 44% compared with negative control (P < 0.05). Moreover, silencing Mct10 mRNA expression abolished the known effects of T3, i.e. suppression of proliferation and enhancement of differentiation, in ATDC5 cells. These results suggest that Mct10 functions as a thyroid hormone transporter in chondrocytes and can explain at least in part why Allan-Herndon-Dudley syndrome patients do not exhibit significant growth impairment.</abstract><cop>Chevy Chase, MD</cop><pub>Endocrine Society</pub><pmid>22719050</pmid><doi>10.1210/en.2011-1713</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences Cell differentiation Cell Line Cell Proliferation Chondrocytes Chondrocytes - cytology Chondrocytes - metabolism Chondrogenesis Differentiation Fundamental and applied biological sciences. Psychology Gene expression Growth plate Hypothyroidism In Situ Hybridization Intellectual disabilities Membrane Transport Proteins - genetics Membrane Transport Proteins - metabolism Mice Mice, Inbred C57BL Monocarboxylic Acid Transporters - genetics Monocarboxylic Acid Transporters - metabolism RNA, Small Interfering siRNA Thyroid Thyroid gland Thyroid Hormones - metabolism Triiodothyronine Vertebrates: endocrinology |
| title | Monocarboxylate Transporter 10 Functions as a Thyroid Hormone Transporter in Chondrocytes |
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