Androgen actions on the human hair follicle: perspectives
Androgens stimulate beard growth but suppress hair growth in androgenetic alopecia (AGA). This condition is known as ‘androgen paradox’. Human pilosebaceous units possess enough enzymes to form the active androgens testosterone and dihydrotestosterone. In hair follicles, 5α‐reductase type 1 and 2, a...
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Veröffentlicht in: | Experimental dermatology 2013-03, Vol.22 (3), p.168-171 |
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creator | Inui, Shigeki Itami, Satoshi |
description | Androgens stimulate beard growth but suppress hair growth in androgenetic alopecia (AGA). This condition is known as ‘androgen paradox’. Human pilosebaceous units possess enough enzymes to form the active androgens testosterone and dihydrotestosterone. In hair follicles, 5α‐reductase type 1 and 2, androgen receptors (AR) and AR coactivators can regulate androgen sensitivity of dermal papillae (DP). To regulate hair growth, androgens stimulate production of IGF‐1 as positive mediators from beard DP cells and of TGF‐β1, TGF‐β2, dickkopf1 and IL‐6 as negative mediators from balding DP cells. In addition, androgens enhance inducible nitric oxide synthase from occipital DP cells and stem cell factor for positive regulation of hair growth in beard and negative regulation of balding DP cells. Moreover, AGA involves crosstalk between androgen and Wnt/β‐catenin signalling. Finally, recent data on susceptibility genes have provided us with the impetus to investigate the molecular pathogenesis of AGA. |
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This condition is known as ‘androgen paradox’. Human pilosebaceous units possess enough enzymes to form the active androgens testosterone and dihydrotestosterone. In hair follicles, 5α‐reductase type 1 and 2, androgen receptors (AR) and AR coactivators can regulate androgen sensitivity of dermal papillae (DP). To regulate hair growth, androgens stimulate production of IGF‐1 as positive mediators from beard DP cells and of TGF‐β1, TGF‐β2, dickkopf1 and IL‐6 as negative mediators from balding DP cells. In addition, androgens enhance inducible nitric oxide synthase from occipital DP cells and stem cell factor for positive regulation of hair growth in beard and negative regulation of balding DP cells. Moreover, AGA involves crosstalk between androgen and Wnt/β‐catenin signalling. Finally, recent data on susceptibility genes have provided us with the impetus to investigate the molecular pathogenesis of AGA.</description><identifier>ISSN: 0906-6705</identifier><identifier>EISSN: 1600-0625</identifier><identifier>DOI: 10.1111/exd.12024</identifier><identifier>PMID: 23016593</identifier><language>eng</language><publisher>Denmark: Blackwell Publishing Ltd</publisher><subject>3-Oxo-5-alpha-Steroid 4-Dehydrogenase - physiology ; 5α-reductase ; androgen ; androgen receptor ; Androgens - physiology ; beta Catenin - physiology ; growth factor ; Hair Follicle - growth & development ; Hair Follicle - physiology ; Humans ; Receptors, Androgen - physiology ; Signal Transduction - physiology ; Wnt ; Wnt Proteins - physiology</subject><ispartof>Experimental dermatology, 2013-03, Vol.22 (3), p.168-171</ispartof><rights>2012 John Wiley & Sons A/S</rights><rights>2012 John Wiley & Sons A/S.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4644-3bd858f6cc1d704100a2d1662e623dc7cd1a45dbc368123fd8aa72a6b2ad9a343</citedby><cites>FETCH-LOGICAL-c4644-3bd858f6cc1d704100a2d1662e623dc7cd1a45dbc368123fd8aa72a6b2ad9a343</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fexd.12024$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fexd.12024$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,782,786,1419,27931,27932,45581,45582</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23016593$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Inui, Shigeki</creatorcontrib><creatorcontrib>Itami, Satoshi</creatorcontrib><title>Androgen actions on the human hair follicle: perspectives</title><title>Experimental dermatology</title><addtitle>Exp Dermatol</addtitle><description>Androgens stimulate beard growth but suppress hair growth in androgenetic alopecia (AGA). This condition is known as ‘androgen paradox’. Human pilosebaceous units possess enough enzymes to form the active androgens testosterone and dihydrotestosterone. In hair follicles, 5α‐reductase type 1 and 2, androgen receptors (AR) and AR coactivators can regulate androgen sensitivity of dermal papillae (DP). To regulate hair growth, androgens stimulate production of IGF‐1 as positive mediators from beard DP cells and of TGF‐β1, TGF‐β2, dickkopf1 and IL‐6 as negative mediators from balding DP cells. In addition, androgens enhance inducible nitric oxide synthase from occipital DP cells and stem cell factor for positive regulation of hair growth in beard and negative regulation of balding DP cells. Moreover, AGA involves crosstalk between androgen and Wnt/β‐catenin signalling. Finally, recent data on susceptibility genes have provided us with the impetus to investigate the molecular pathogenesis of AGA.</description><subject>3-Oxo-5-alpha-Steroid 4-Dehydrogenase - physiology</subject><subject>5α-reductase</subject><subject>androgen</subject><subject>androgen receptor</subject><subject>Androgens - physiology</subject><subject>beta Catenin - physiology</subject><subject>growth factor</subject><subject>Hair Follicle - growth & development</subject><subject>Hair Follicle - physiology</subject><subject>Humans</subject><subject>Receptors, Androgen - physiology</subject><subject>Signal Transduction - physiology</subject><subject>Wnt</subject><subject>Wnt Proteins - physiology</subject><issn>0906-6705</issn><issn>1600-0625</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kDtPwzAUhS0EoqUw8AdQRhjS-pE4CVsppSAVEBKIbpZj39BAXtgJtP-elNBunOXqSt85w4fQKcFD0mYEKz0kFFNvD_UJx9jFnPr7qI8jzF0eYL-Hjqx9x5gELPAPUY8yTLgfsT6KxoU25RsUjlR1WhbWKQunXoKzbHJZOEuZGicpsyxVGVw6FRhbQQt-gT1GB4nMLJz83QF6uZk-T27d-ePsbjKeu8rjnueyWId-mHCliA6wRzCWVBPOKXDKtAqUJtLzdawYDwlliQ6lDKjkMZU6ksxjA3Te7Vam_GzA1iJPrYIskwWUjRWEkSBkbWiLXnSoMqW1BhJRmTSXZi0IFhtTojUlfk217NnfbBPnoHfkVk0LjDrgO81g_f-SmC6ut5Nu10htDatdQ5oPwTfixevDTFyxp8X95pmzH2rUgEs</recordid><startdate>201303</startdate><enddate>201303</enddate><creator>Inui, Shigeki</creator><creator>Itami, Satoshi</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</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>7X8</scope></search><sort><creationdate>201303</creationdate><title>Androgen actions on the human hair follicle: perspectives</title><author>Inui, Shigeki ; Itami, Satoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4644-3bd858f6cc1d704100a2d1662e623dc7cd1a45dbc368123fd8aa72a6b2ad9a343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>3-Oxo-5-alpha-Steroid 4-Dehydrogenase - physiology</topic><topic>5α-reductase</topic><topic>androgen</topic><topic>androgen receptor</topic><topic>Androgens - physiology</topic><topic>beta Catenin - physiology</topic><topic>growth factor</topic><topic>Hair Follicle - growth & development</topic><topic>Hair Follicle - physiology</topic><topic>Humans</topic><topic>Receptors, Androgen - physiology</topic><topic>Signal Transduction - physiology</topic><topic>Wnt</topic><topic>Wnt Proteins - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Inui, Shigeki</creatorcontrib><creatorcontrib>Itami, Satoshi</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental dermatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Inui, Shigeki</au><au>Itami, Satoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Androgen actions on the human hair follicle: perspectives</atitle><jtitle>Experimental dermatology</jtitle><addtitle>Exp Dermatol</addtitle><date>2013-03</date><risdate>2013</risdate><volume>22</volume><issue>3</issue><spage>168</spage><epage>171</epage><pages>168-171</pages><issn>0906-6705</issn><eissn>1600-0625</eissn><abstract>Androgens stimulate beard growth but suppress hair growth in androgenetic alopecia (AGA). This condition is known as ‘androgen paradox’. Human pilosebaceous units possess enough enzymes to form the active androgens testosterone and dihydrotestosterone. In hair follicles, 5α‐reductase type 1 and 2, androgen receptors (AR) and AR coactivators can regulate androgen sensitivity of dermal papillae (DP). To regulate hair growth, androgens stimulate production of IGF‐1 as positive mediators from beard DP cells and of TGF‐β1, TGF‐β2, dickkopf1 and IL‐6 as negative mediators from balding DP cells. In addition, androgens enhance inducible nitric oxide synthase from occipital DP cells and stem cell factor for positive regulation of hair growth in beard and negative regulation of balding DP cells. Moreover, AGA involves crosstalk between androgen and Wnt/β‐catenin signalling. 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subjects | 3-Oxo-5-alpha-Steroid 4-Dehydrogenase - physiology 5α-reductase androgen androgen receptor Androgens - physiology beta Catenin - physiology growth factor Hair Follicle - growth & development Hair Follicle - physiology Humans Receptors, Androgen - physiology Signal Transduction - physiology Wnt Wnt Proteins - physiology |
title | Androgen actions on the human hair follicle: perspectives |
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