Indications for a brain‐hair follicle axis: inhibition of keratinocyte proliferation and up‐regulation of keratinocyte apoptosis in telogen hair follicles by stress and substance P
ABSTRACT It has long been suspected that stress can cause hair loss, although convincing evidence of this has been unavailable. Here, we show that in mice sonic stress significantly increased the number of hair follicles containing apoptotic cells and inhibited intrafollicular keratinocyte prolifera...
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| Veröffentlicht in: | The FASEB journal 2001-11, Vol.15 (13), p.2536-2538 |
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| creator | Arck, Petra Clara Handjiski, Bori Hagen, Evelin Joachim, Ricarda Klapp, Burghard F. Paus, Ralf |
| description | ABSTRACT
It has long been suspected that stress can cause hair loss, although convincing evidence of this has been unavailable. Here, we show that in mice sonic stress significantly increased the number of hair follicles containing apoptotic cells and inhibited intrafollicular keratinocyte proliferation in situ. Sonic stress also significantly increased the number of activated perifollicular macrophage clusters and the number of degranulated mast cells, whereas it down‐regulated the number of intraepithelial γδ T lymphocytes. These stress‐induced immune changes could be mimicked by injection of the neuropeptide substance P in nonstressed mice and were abrogated by a selective substance P receptor antagonist in stressed mice. We conclude that stress can indeed inhibit hair growth in vivo, probably via a substance P‐dependent activation of macrophages and/or mast cells in the context of a brain‐hair follicle axis. |
| doi_str_mv | 10.1096/fj.00-0699fje |
| format | Article |
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It has long been suspected that stress can cause hair loss, although convincing evidence of this has been unavailable. Here, we show that in mice sonic stress significantly increased the number of hair follicles containing apoptotic cells and inhibited intrafollicular keratinocyte proliferation in situ. Sonic stress also significantly increased the number of activated perifollicular macrophage clusters and the number of degranulated mast cells, whereas it down‐regulated the number of intraepithelial γδ T lymphocytes. These stress‐induced immune changes could be mimicked by injection of the neuropeptide substance P in nonstressed mice and were abrogated by a selective substance P receptor antagonist in stressed mice. We conclude that stress can indeed inhibit hair growth in vivo, probably via a substance P‐dependent activation of macrophages and/or mast cells in the context of a brain‐hair follicle axis.</description><identifier>ISSN: 0892-6638</identifier><identifier>EISSN: 1530-6860</identifier><identifier>DOI: 10.1096/fj.00-0699fje</identifier><identifier>PMID: 11641256</identifier><language>eng</language><publisher>United States: Federation of American Societies for Experimental Biology</publisher><subject>Acoustic Stimulation ; activated macrophages ; Animals ; apoptosis ; Apoptosis - drug effects ; Brain - physiology ; Cell Degranulation ; Cell Division - drug effects ; Cytokines - biosynthesis ; hair follicle ; Hair Follicle - chemistry ; Hair Follicle - drug effects ; Hair Follicle - growth & development ; Histocompatibility Antigens Class II - biosynthesis ; Immunohistochemistry ; In Situ Nick-End Labeling ; Indoles - pharmacology ; Isoindoles ; Keratinocytes - chemistry ; Keratinocytes - cytology ; Keratinocytes - drug effects ; Ki-67 Antigen - analysis ; Macrophages - metabolism ; Macrophages - pathology ; mast cells ; Mast Cells - physiology ; Mice ; Receptors, Antigen, T-Cell, gamma-delta - biosynthesis ; Skin - metabolism ; Skin - pathology ; sonic stress ; Stress, Physiological - physiopathology ; Substance P - pharmacology ; T-Lymphocytes - cytology ; T-Lymphocytes - metabolism ; Up-Regulation</subject><ispartof>The FASEB journal, 2001-11, Vol.15 (13), p.2536-2538</ispartof><rights>FASEB</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c437E-defed05f9e2f0d4e0f39db3b7165cd8153f77a480a013b3a77be019de141178b3</citedby><cites>FETCH-LOGICAL-c437E-defed05f9e2f0d4e0f39db3b7165cd8153f77a480a013b3a77be019de141178b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1096%2Ffj.00-0699fje$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1096%2Ffj.00-0699fje$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,778,782,1414,27907,27908,45557,45558</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11641256$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Arck, Petra Clara</creatorcontrib><creatorcontrib>Handjiski, Bori</creatorcontrib><creatorcontrib>Hagen, Evelin</creatorcontrib><creatorcontrib>Joachim, Ricarda</creatorcontrib><creatorcontrib>Klapp, Burghard F.</creatorcontrib><creatorcontrib>Paus, Ralf</creatorcontrib><title>Indications for a brain‐hair follicle axis: inhibition of keratinocyte proliferation and up‐regulation of keratinocyte apoptosis in telogen hair follicles by stress and substance P</title><title>The FASEB journal</title><addtitle>FASEB J</addtitle><description>ABSTRACT
It has long been suspected that stress can cause hair loss, although convincing evidence of this has been unavailable. Here, we show that in mice sonic stress significantly increased the number of hair follicles containing apoptotic cells and inhibited intrafollicular keratinocyte proliferation in situ. Sonic stress also significantly increased the number of activated perifollicular macrophage clusters and the number of degranulated mast cells, whereas it down‐regulated the number of intraepithelial γδ T lymphocytes. These stress‐induced immune changes could be mimicked by injection of the neuropeptide substance P in nonstressed mice and were abrogated by a selective substance P receptor antagonist in stressed mice. We conclude that stress can indeed inhibit hair growth in vivo, probably via a substance P‐dependent activation of macrophages and/or mast cells in the context of a brain‐hair follicle axis.</description><subject>Acoustic Stimulation</subject><subject>activated macrophages</subject><subject>Animals</subject><subject>apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Brain - physiology</subject><subject>Cell Degranulation</subject><subject>Cell Division - drug effects</subject><subject>Cytokines - biosynthesis</subject><subject>hair follicle</subject><subject>Hair Follicle - chemistry</subject><subject>Hair Follicle - drug effects</subject><subject>Hair Follicle - growth & development</subject><subject>Histocompatibility Antigens Class II - biosynthesis</subject><subject>Immunohistochemistry</subject><subject>In Situ Nick-End Labeling</subject><subject>Indoles - pharmacology</subject><subject>Isoindoles</subject><subject>Keratinocytes - chemistry</subject><subject>Keratinocytes - cytology</subject><subject>Keratinocytes - drug effects</subject><subject>Ki-67 Antigen - analysis</subject><subject>Macrophages - metabolism</subject><subject>Macrophages - pathology</subject><subject>mast cells</subject><subject>Mast Cells - physiology</subject><subject>Mice</subject><subject>Receptors, Antigen, T-Cell, gamma-delta - biosynthesis</subject><subject>Skin - metabolism</subject><subject>Skin - pathology</subject><subject>sonic stress</subject><subject>Stress, Physiological - physiopathology</subject><subject>Substance P - pharmacology</subject><subject>T-Lymphocytes - cytology</subject><subject>T-Lymphocytes - metabolism</subject><subject>Up-Regulation</subject><issn>0892-6638</issn><issn>1530-6860</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFksFu1DAQhi0EokvhyBX5xC1lHCdO0htUu9CqUpGAs2Un49aL1w52IthbH6GPw_PwJHi7KyEkVE6Wx998I_s3IS8ZnDDoxBuzPgEoQHSdWeMjsmA1h0K0Ah6TBbRdWQjB2yPyLKU1ADBg4ik5YkxUrKzFgvw894Pt1WSDT9SESBXVUVn_6_buRtmYS87Z3iFVP2w6pdbfWG13NA2GfsWYO33otxPSMQZnzX0lnyo_0HnMlojXs1P_7FBjGKeQbMpaOqEL1-jpX1MT1Vuapogp3RvTrNOkfI_043PyxCiX8MVhPSZfVsvPZx-Ky6v352dvL4u-4s2yGNDgALXpsDQwVAiGd4PmumGi7oc2v5ZpGlW1oIBxzVXTaATWDcgqxppW82Pyeu_N9_s2Y5rkxqYenVMew5xkU5Z1zUv2X5A1u7xansFiD_YxpBTRyDHajYpbyUDuGGnWEkAeMs38q4N41hsc_tCHEDNwuge-W4fbh21y9eldubrIXyHvVxdL_hskS7bF</recordid><startdate>200111</startdate><enddate>200111</enddate><creator>Arck, Petra Clara</creator><creator>Handjiski, Bori</creator><creator>Hagen, Evelin</creator><creator>Joachim, Ricarda</creator><creator>Klapp, Burghard F.</creator><creator>Paus, Ralf</creator><general>Federation of American Societies for Experimental Biology</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>7TK</scope><scope>7X8</scope></search><sort><creationdate>200111</creationdate><title>Indications for a brain‐hair follicle axis: inhibition of keratinocyte proliferation and up‐regulation of keratinocyte apoptosis in telogen hair follicles by stress and substance P</title><author>Arck, Petra Clara ; Handjiski, Bori ; Hagen, Evelin ; Joachim, Ricarda ; Klapp, Burghard F. ; Paus, Ralf</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c437E-defed05f9e2f0d4e0f39db3b7165cd8153f77a480a013b3a77be019de141178b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Acoustic Stimulation</topic><topic>activated macrophages</topic><topic>Animals</topic><topic>apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Brain - physiology</topic><topic>Cell Degranulation</topic><topic>Cell Division - drug effects</topic><topic>Cytokines - biosynthesis</topic><topic>hair follicle</topic><topic>Hair Follicle - chemistry</topic><topic>Hair Follicle - drug effects</topic><topic>Hair Follicle - growth & development</topic><topic>Histocompatibility Antigens Class II - biosynthesis</topic><topic>Immunohistochemistry</topic><topic>In Situ Nick-End Labeling</topic><topic>Indoles - pharmacology</topic><topic>Isoindoles</topic><topic>Keratinocytes - chemistry</topic><topic>Keratinocytes - cytology</topic><topic>Keratinocytes - drug effects</topic><topic>Ki-67 Antigen - analysis</topic><topic>Macrophages - metabolism</topic><topic>Macrophages - pathology</topic><topic>mast cells</topic><topic>Mast Cells - physiology</topic><topic>Mice</topic><topic>Receptors, Antigen, T-Cell, gamma-delta - biosynthesis</topic><topic>Skin - metabolism</topic><topic>Skin - pathology</topic><topic>sonic stress</topic><topic>Stress, Physiological - physiopathology</topic><topic>Substance P - pharmacology</topic><topic>T-Lymphocytes - cytology</topic><topic>T-Lymphocytes - metabolism</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Arck, Petra Clara</creatorcontrib><creatorcontrib>Handjiski, Bori</creatorcontrib><creatorcontrib>Hagen, Evelin</creatorcontrib><creatorcontrib>Joachim, Ricarda</creatorcontrib><creatorcontrib>Klapp, Burghard F.</creatorcontrib><creatorcontrib>Paus, Ralf</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The FASEB journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Arck, Petra Clara</au><au>Handjiski, Bori</au><au>Hagen, Evelin</au><au>Joachim, Ricarda</au><au>Klapp, Burghard F.</au><au>Paus, Ralf</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Indications for a brain‐hair follicle axis: inhibition of keratinocyte proliferation and up‐regulation of keratinocyte apoptosis in telogen hair follicles by stress and substance P</atitle><jtitle>The FASEB journal</jtitle><addtitle>FASEB J</addtitle><date>2001-11</date><risdate>2001</risdate><volume>15</volume><issue>13</issue><spage>2536</spage><epage>2538</epage><pages>2536-2538</pages><issn>0892-6638</issn><eissn>1530-6860</eissn><abstract>ABSTRACT
It has long been suspected that stress can cause hair loss, although convincing evidence of this has been unavailable. Here, we show that in mice sonic stress significantly increased the number of hair follicles containing apoptotic cells and inhibited intrafollicular keratinocyte proliferation in situ. Sonic stress also significantly increased the number of activated perifollicular macrophage clusters and the number of degranulated mast cells, whereas it down‐regulated the number of intraepithelial γδ T lymphocytes. These stress‐induced immune changes could be mimicked by injection of the neuropeptide substance P in nonstressed mice and were abrogated by a selective substance P receptor antagonist in stressed mice. We conclude that stress can indeed inhibit hair growth in vivo, probably via a substance P‐dependent activation of macrophages and/or mast cells in the context of a brain‐hair follicle axis.</abstract><cop>United States</cop><pub>Federation of American Societies for Experimental Biology</pub><pmid>11641256</pmid><doi>10.1096/fj.00-0699fje</doi><tpages>26</tpages></addata></record> |
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| subjects | Acoustic Stimulation activated macrophages Animals apoptosis Apoptosis - drug effects Brain - physiology Cell Degranulation Cell Division - drug effects Cytokines - biosynthesis hair follicle Hair Follicle - chemistry Hair Follicle - drug effects Hair Follicle - growth & development Histocompatibility Antigens Class II - biosynthesis Immunohistochemistry In Situ Nick-End Labeling Indoles - pharmacology Isoindoles Keratinocytes - chemistry Keratinocytes - cytology Keratinocytes - drug effects Ki-67 Antigen - analysis Macrophages - metabolism Macrophages - pathology mast cells Mast Cells - physiology Mice Receptors, Antigen, T-Cell, gamma-delta - biosynthesis Skin - metabolism Skin - pathology sonic stress Stress, Physiological - physiopathology Substance P - pharmacology T-Lymphocytes - cytology T-Lymphocytes - metabolism Up-Regulation |
| title | Indications for a brain‐hair follicle axis: inhibition of keratinocyte proliferation and up‐regulation of keratinocyte apoptosis in telogen hair follicles by stress and substance P |
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