Gsdma3 gene is needed for the induction of apoptosis-driven catagen during mouse hair follicle cycle
Gsdm is a newly found gene family, which is restricted in its expression to the gastrointestinal tract and the skin epithelium. As a main member of the Gsdma subfamily, Gsdma3 is expressed specifically in the hair follicle of mouse skin, but its function remains largely unclear. By hematoxylin and e...
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description | Gsdm
is a newly found gene family, which is restricted in its expression to the gastrointestinal tract and the skin epithelium. As a main member of the
Gsdma
subfamily,
Gsdma3
is expressed specifically in the hair follicle of mouse skin, but its function remains largely unclear. By hematoxylin and eosin staining, we showed that
Gsdma3
gene mutation caused an abnormal catagen phase with unshortened length and unshrunk structure of the hair follicle, in which the development of catagen phase was inhibited. TUNEL staining further revealed that the apoptosis of the hair follicle was obviously decreased in mutant mice.
Caspase
-
3
downregulation was also detected by immunofluorescence, Western blot and RT-PCR in the hair follicle of the mutant mice. After intradermal injection of
Gsdma3
gene expression plasmid, apoptosis as well as
Caspase
-
3
expression in the hair follicle of mutant mice was enhanced, and so the catagen retardation of
Gsdma3
-mutant mice was rescued. Our results confirmed that
Gsdma3
gene mutation interfered with catagen formation during mouse hair follicle cycle and, by upregulation of
Caspase
-
3
expression and promotion of apoptosis,
Gsdma3
gene could play an essential role in normal catagen induction. |
doi_str_mv | 10.1007/s00418-011-0845-8 |
format | Article |
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is a newly found gene family, which is restricted in its expression to the gastrointestinal tract and the skin epithelium. As a main member of the
Gsdma
subfamily,
Gsdma3
is expressed specifically in the hair follicle of mouse skin, but its function remains largely unclear. By hematoxylin and eosin staining, we showed that
Gsdma3
gene mutation caused an abnormal catagen phase with unshortened length and unshrunk structure of the hair follicle, in which the development of catagen phase was inhibited. TUNEL staining further revealed that the apoptosis of the hair follicle was obviously decreased in mutant mice.
Caspase
-
3
downregulation was also detected by immunofluorescence, Western blot and RT-PCR in the hair follicle of the mutant mice. After intradermal injection of
Gsdma3
gene expression plasmid, apoptosis as well as
Caspase
-
3
expression in the hair follicle of mutant mice was enhanced, and so the catagen retardation of
Gsdma3
-mutant mice was rescued. Our results confirmed that
Gsdma3
gene mutation interfered with catagen formation during mouse hair follicle cycle and, by upregulation of
Caspase
-
3
expression and promotion of apoptosis,
Gsdma3
gene could play an essential role in normal catagen induction.</description><identifier>ISSN: 0948-6143</identifier><identifier>EISSN: 1432-119X</identifier><identifier>DOI: 10.1007/s00418-011-0845-8</identifier><identifier>PMID: 21805153</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Animals ; Apoptosis ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Caspase 3 - genetics ; Caspase 3 - metabolism ; Cell Biology ; Developmental Biology ; Enzymes ; Fluorescent Antibody Technique ; Gene expression ; Hair ; Hair Follicle - cytology ; Hair Follicle - physiology ; Mice ; Mice, Mutant Strains ; Original Paper ; Proteins - genetics ; Proteins - metabolism ; Rodents ; Up-Regulation</subject><ispartof>Histochemistry and cell biology, 2011-09, Vol.136 (3), p.335-343</ispartof><rights>Springer-Verlag 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c436t-90c80539efe62a8a48a93c62286d58def0321ac26bed1905d21dc6e9a5fb0ac3</citedby><cites>FETCH-LOGICAL-c436t-90c80539efe62a8a48a93c62286d58def0321ac26bed1905d21dc6e9a5fb0ac3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00418-011-0845-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00418-011-0845-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21805153$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lei, Mingxing</creatorcontrib><creatorcontrib>Gao, Xiang</creatorcontrib><creatorcontrib>Yang, Li</creatorcontrib><creatorcontrib>Yang, Tian</creatorcontrib><creatorcontrib>Lian, Xiaohua</creatorcontrib><title>Gsdma3 gene is needed for the induction of apoptosis-driven catagen during mouse hair follicle cycle</title><title>Histochemistry and cell biology</title><addtitle>Histochem Cell Biol</addtitle><addtitle>Histochem Cell Biol</addtitle><description>Gsdm
is a newly found gene family, which is restricted in its expression to the gastrointestinal tract and the skin epithelium. As a main member of the
Gsdma
subfamily,
Gsdma3
is expressed specifically in the hair follicle of mouse skin, but its function remains largely unclear. By hematoxylin and eosin staining, we showed that
Gsdma3
gene mutation caused an abnormal catagen phase with unshortened length and unshrunk structure of the hair follicle, in which the development of catagen phase was inhibited. TUNEL staining further revealed that the apoptosis of the hair follicle was obviously decreased in mutant mice.
Caspase
-
3
downregulation was also detected by immunofluorescence, Western blot and RT-PCR in the hair follicle of the mutant mice. After intradermal injection of
Gsdma3
gene expression plasmid, apoptosis as well as
Caspase
-
3
expression in the hair follicle of mutant mice was enhanced, and so the catagen retardation of
Gsdma3
-mutant mice was rescued. Our results confirmed that
Gsdma3
gene mutation interfered with catagen formation during mouse hair follicle cycle and, by upregulation of
Caspase
-
3
expression and promotion of apoptosis,
Gsdma3
gene could play an essential role in normal catagen induction.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Caspase 3 - genetics</subject><subject>Caspase 3 - metabolism</subject><subject>Cell Biology</subject><subject>Developmental Biology</subject><subject>Enzymes</subject><subject>Fluorescent Antibody Technique</subject><subject>Gene expression</subject><subject>Hair</subject><subject>Hair Follicle - cytology</subject><subject>Hair Follicle - physiology</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Original Paper</subject><subject>Proteins - genetics</subject><subject>Proteins - metabolism</subject><subject>Rodents</subject><subject>Up-Regulation</subject><issn>0948-6143</issn><issn>1432-119X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kMFq3DAQhkVoyG6TPEAuRfTSkxKNLLnSsSzpNhDoJYfchFYaJ1psy5XsQt6-WjZpoNCLBobvH_18hFwBvwbOv94UziVoxgEY11IxfULWIBvBAMzjB7LmRmrW1s2KfCxlzzkoI8QZWQnQXIFq1iRsSxhcQ59wRBoLHREDBtqlTOfnuhnD4ueYRpo66qY0zanEwkKOv3Gk3s2uBmlYchyf6JCWgvTZxVzzfR99j9S_1PeCnHauL3j5Os_Jw_fbh80Pdv9ze7f5ds-8bNqZGe5rrcZgh61w2kntTONbIXQblA7Y8UaA86LdYQDDVRAQfIvGqW7HnW_OyZfj2SmnXwuW2Q6xeOx7N2KtZrWWWhqhVCU__0Pu05LH2u0ASd0KAxWCI-RzKiVjZ6ccB5dfLHB78G-P_m31bw_-ra6ZT6-Hl92A4W_iTXgFxBEo08EZ5vef_3_1DxTmkIo</recordid><startdate>20110901</startdate><enddate>20110901</enddate><creator>Lei, Mingxing</creator><creator>Gao, Xiang</creator><creator>Yang, Li</creator><creator>Yang, Tian</creator><creator>Lian, Xiaohua</creator><general>Springer-Verlag</general><general>Springer Nature B.V</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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</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>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20110901</creationdate><title>Gsdma3 gene is needed for the induction of apoptosis-driven catagen during mouse hair follicle cycle</title><author>Lei, Mingxing ; Gao, Xiang ; Yang, Li ; Yang, Tian ; Lian, Xiaohua</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c436t-90c80539efe62a8a48a93c62286d58def0321ac26bed1905d21dc6e9a5fb0ac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Caspase 3 - genetics</topic><topic>Caspase 3 - metabolism</topic><topic>Cell Biology</topic><topic>Developmental Biology</topic><topic>Enzymes</topic><topic>Fluorescent Antibody Technique</topic><topic>Gene expression</topic><topic>Hair</topic><topic>Hair Follicle - cytology</topic><topic>Hair Follicle - physiology</topic><topic>Mice</topic><topic>Mice, Mutant Strains</topic><topic>Original Paper</topic><topic>Proteins - genetics</topic><topic>Proteins - metabolism</topic><topic>Rodents</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lei, Mingxing</creatorcontrib><creatorcontrib>Gao, Xiang</creatorcontrib><creatorcontrib>Yang, Li</creatorcontrib><creatorcontrib>Yang, Tian</creatorcontrib><creatorcontrib>Lian, Xiaohua</creatorcontrib><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>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</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>ProQuest Pharma Collection</collection><collection>Public Health 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>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>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</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>MEDLINE - Academic</collection><jtitle>Histochemistry and cell biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lei, Mingxing</au><au>Gao, Xiang</au><au>Yang, Li</au><au>Yang, Tian</au><au>Lian, Xiaohua</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gsdma3 gene is needed for the induction of apoptosis-driven catagen during mouse hair follicle cycle</atitle><jtitle>Histochemistry and cell biology</jtitle><stitle>Histochem Cell Biol</stitle><addtitle>Histochem Cell Biol</addtitle><date>2011-09-01</date><risdate>2011</risdate><volume>136</volume><issue>3</issue><spage>335</spage><epage>343</epage><pages>335-343</pages><issn>0948-6143</issn><eissn>1432-119X</eissn><abstract>Gsdm
is a newly found gene family, which is restricted in its expression to the gastrointestinal tract and the skin epithelium. As a main member of the
Gsdma
subfamily,
Gsdma3
is expressed specifically in the hair follicle of mouse skin, but its function remains largely unclear. By hematoxylin and eosin staining, we showed that
Gsdma3
gene mutation caused an abnormal catagen phase with unshortened length and unshrunk structure of the hair follicle, in which the development of catagen phase was inhibited. TUNEL staining further revealed that the apoptosis of the hair follicle was obviously decreased in mutant mice.
Caspase
-
3
downregulation was also detected by immunofluorescence, Western blot and RT-PCR in the hair follicle of the mutant mice. After intradermal injection of
Gsdma3
gene expression plasmid, apoptosis as well as
Caspase
-
3
expression in the hair follicle of mutant mice was enhanced, and so the catagen retardation of
Gsdma3
-mutant mice was rescued. Our results confirmed that
Gsdma3
gene mutation interfered with catagen formation during mouse hair follicle cycle and, by upregulation of
Caspase
-
3
expression and promotion of apoptosis,
Gsdma3
gene could play an essential role in normal catagen induction.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>21805153</pmid><doi>10.1007/s00418-011-0845-8</doi><tpages>9</tpages></addata></record> |
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language | eng |
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source | MEDLINE; SpringerLink Journals - AutoHoldings |
subjects | Animals Apoptosis Biochemistry Biomedical and Life Sciences Biomedicine Caspase 3 - genetics Caspase 3 - metabolism Cell Biology Developmental Biology Enzymes Fluorescent Antibody Technique Gene expression Hair Hair Follicle - cytology Hair Follicle - physiology Mice Mice, Mutant Strains Original Paper Proteins - genetics Proteins - metabolism Rodents Up-Regulation |
title | Gsdma3 gene is needed for the induction of apoptosis-driven catagen during mouse hair follicle cycle |
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