Sexual hormones utilize complex mechanisms to modulate sebocyte differentiation
Identifieur interne : 001904 ( Istex/Corpus ); précédent : 001903; suivant : 001905Sexual hormones utilize complex mechanisms to modulate sebocyte differentiation
Auteurs : Chc Zouboulis ; W. Chen ; Th. Alestas ; E. Makrantonaki ; H. Seltmann ; K. Müller-DeckerSource :
- Experimental Dermatology [ 0906-6705 ] ; 2005-02.
English descriptors
- Teeft :
- Acth, Androgen, Androgen activity, Antisense oligonucleotides, Atopic dermatitis, Basal serum levels, Biomedical sciences, Calcitriol, Calcitriol synthesis, Campus benjamin franklin, Carl gustav carus, Cell biology, Cell growth, Cholinergic agonists, Clinical monitoring, Collagen synthesis, Complex mechanisms, Connective tissue sheath fibroblasts, Cultured keratinocytes, Cutaneous, Dermal microvascular, Dermal papilla cells, Dermatology, Dresden university, Environmental dermatology, Epidermal, Epidermal differentiation, Epidermal hydration, Epidermal keratinocytes, Epidermis, Epithelial cells, Estrogen, Extracellular matrix, Fibroblast, First time, Follicle, Foreskin keratinocytes, Functional significance, Hair cycle dependence, Hair follicle, Hair follicle biology, Hdmec membranes, Human ache, Human epidermis, Human hair follicles, Human keratinocytes, Human skin, Immunoreactivity, Important role, Inhibitor, Keratinocyte differentiation, Keratinocytes, Local production, Local synthesis, Ludwig boltzmann institute, Malignant melanoma, Mammalian skin, Melanocortin receptors, Melanoma, Melanoma cell lines, Melanoma cells, Melatonin, Munster, Murine hair follicles, Narrowband lamp, Normal skin, Oligonucleotides, Organotypic cultures, Other hand, Oxidative stress, Oxysterols, Pomc, Pomc peptides, Postmenopausal women, Prurigo nodularis, Psoriasis vulgaris, Radical scavenger, Real time, Receptor, Recovery time, Sebaceous, Sebaceous lipogenesis, Sebocyte differentiation, Sexual hormones, Side effects, Skin surface lipids, Splice variants, Such treatment, Terminal differentiation, Tumor necrosis, Vanilloid receptor subtype, Various cell types, Various melanoma cell lines, Various studies, Vitamin growth inhibition, Wahringer gurtel vienna, Western blot analysis, Wolfgang tilgen1, Wound healing.
Abstract
Sexual hormones are important in the maintenance of human skin. Being the endocrine “brain” of the skin, the sebaceous gland is a major target of sexual hormones. While androgens stimulate sebocyte proliferation, estrogens do not to affect sebaceous gland growth. Regarding differentiation, androgens are expected to stimulate and estrogens to suppress sebaceous lipid synthesis, while estrogens, in vivo, enhance sebaceous lipogenesis in aged skin. The latter results have been disputed by current in vitro data indicating no direct effect of sexual hormones on sebocyte differentiation. To elucidate these contradictions we have investigated possible pathways which may be used by sexual hormones to modulate sebocyte differentiation in vitro. It has been postulated that androgen induction of lipogenesis requires the concomitant presence of peroxisome proliferator‐activated receptor (PPAR) ligands. We found that arachidonic acid (AA), the direct precursor of leukotriene B4, a natural PPARα ligand, and linoleic acid (LA), a natural PPARδ ligand, induce sebocyte enlargement, accumulation of lipid droplets in the cytoplasm, and nuclear fragmentation. The combined administration of testosterone and AA or LA slightly increased sebaceous lipogenesis. In contrast, synthetic PPAR ligands were unable to enhance sebaceous lipogenesis. Interestingly, AA synthesis in human sebocytes was significantly stimulated by the prostaglandins (PG) E2 and Δ15‐J2. On the other hand, PPARγ expression was downregulated by the phytoestrogen genistein. Interestingly, 17β‐estradiol has previously been shown to induce the metabolism of PGD2 to Δ12‐PGJ2, a natural PPARγ ligand. In addition, we found that 17β‐estradiol increases IGF‐I synthesis (+28%) and down‐regulates IGF‐IR expression (−37 to −48%), whereas IGF‐I significantly induces sebaceous lipogenesis. In conclusion, sexual hormones are not directly active but are likely to utilize complex mechanisms, including modified known pro‐inflammatory pathways, to modulate sebocyte differentiation.
Url:
DOI: 10.1111/j.0906-6705.2005.0266l.x
Links to Exploration step
ISTEX:EF0FB3B9BE0DC5E158A7FFE0036F3D7951685A9ELe document en format XML
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Müller-Decker</name><affiliation><mods:affiliation>Department of Dermatology, Campus Benjamin Franklin, Charité– Universitaetsmedizin Berlin, Berlin, and §Eicosanoids and Epithelial Tumor Development Research Group, Deutsches Krebsforschungszentrum, Heidelberg, Germany, and *Department of Dermatology, Chang Gung University, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Experimental Dermatology</title><idno type="ISSN">0906-6705</idno><idno type="eISSN">1600-0625</idno><imprint><publisher>Munksgaard International Publishers</publisher><pubPlace>Oxford, UK; Malden, USA</pubPlace><date type="published" when="2005-02">2005-02</date><biblScope unit="volume">14</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="156">156</biblScope><biblScope unit="page" to="156">156</biblScope></imprint><idno type="ISSN">0906-6705</idno></series><idno type="istex">EF0FB3B9BE0DC5E158A7FFE0036F3D7951685A9E</idno><idno type="DOI">10.1111/j.0906-6705.2005.0266l.x</idno><idno type="ArticleID">EXD266L</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0906-6705</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Acth</term><term>Androgen</term><term>Androgen activity</term><term>Antisense oligonucleotides</term><term>Atopic dermatitis</term><term>Basal serum levels</term><term>Biomedical sciences</term><term>Calcitriol</term><term>Calcitriol synthesis</term><term>Campus benjamin franklin</term><term>Carl gustav carus</term><term>Cell biology</term><term>Cell growth</term><term>Cholinergic agonists</term><term>Clinical monitoring</term><term>Collagen synthesis</term><term>Complex mechanisms</term><term>Connective tissue sheath fibroblasts</term><term>Cultured keratinocytes</term><term>Cutaneous</term><term>Dermal microvascular</term><term>Dermal papilla cells</term><term>Dermatology</term><term>Dresden university</term><term>Environmental dermatology</term><term>Epidermal</term><term>Epidermal differentiation</term><term>Epidermal hydration</term><term>Epidermal keratinocytes</term><term>Epidermis</term><term>Epithelial cells</term><term>Estrogen</term><term>Extracellular matrix</term><term>Fibroblast</term><term>First time</term><term>Follicle</term><term>Foreskin keratinocytes</term><term>Functional significance</term><term>Hair cycle dependence</term><term>Hair follicle</term><term>Hair follicle biology</term><term>Hdmec membranes</term><term>Human ache</term><term>Human epidermis</term><term>Human hair follicles</term><term>Human keratinocytes</term><term>Human skin</term><term>Immunoreactivity</term><term>Important role</term><term>Inhibitor</term><term>Keratinocyte differentiation</term><term>Keratinocytes</term><term>Local production</term><term>Local synthesis</term><term>Ludwig boltzmann institute</term><term>Malignant melanoma</term><term>Mammalian skin</term><term>Melanocortin receptors</term><term>Melanoma</term><term>Melanoma cell lines</term><term>Melanoma cells</term><term>Melatonin</term><term>Munster</term><term>Murine hair follicles</term><term>Narrowband lamp</term><term>Normal skin</term><term>Oligonucleotides</term><term>Organotypic cultures</term><term>Other hand</term><term>Oxidative stress</term><term>Oxysterols</term><term>Pomc</term><term>Pomc peptides</term><term>Postmenopausal women</term><term>Prurigo nodularis</term><term>Psoriasis vulgaris</term><term>Radical scavenger</term><term>Real time</term><term>Receptor</term><term>Recovery time</term><term>Sebaceous</term><term>Sebaceous lipogenesis</term><term>Sebocyte differentiation</term><term>Sexual hormones</term><term>Side effects</term><term>Skin surface lipids</term><term>Splice variants</term><term>Such treatment</term><term>Terminal differentiation</term><term>Tumor necrosis</term><term>Vanilloid receptor subtype</term><term>Various cell types</term><term>Various melanoma cell lines</term><term>Various studies</term><term>Vitamin growth inhibition</term><term>Wahringer gurtel vienna</term><term>Western blot analysis</term><term>Wolfgang tilgen1</term><term>Wound healing</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Sexual hormones are important in the maintenance of human skin. Being the endocrine “brain” of the skin, the sebaceous gland is a major target of sexual hormones. While androgens stimulate sebocyte proliferation, estrogens do not to affect sebaceous gland growth. Regarding differentiation, androgens are expected to stimulate and estrogens to suppress sebaceous lipid synthesis, while estrogens, in vivo, enhance sebaceous lipogenesis in aged skin. The latter results have been disputed by current in vitro data indicating no direct effect of sexual hormones on sebocyte differentiation. To elucidate these contradictions we have investigated possible pathways which may be used by sexual hormones to modulate sebocyte differentiation in vitro. It has been postulated that androgen induction of lipogenesis requires the concomitant presence of peroxisome proliferator‐activated receptor (PPAR) ligands. We found that arachidonic acid (AA), the direct precursor of leukotriene B4, a natural PPARα ligand, and linoleic acid (LA), a natural PPARδ ligand, induce sebocyte enlargement, accumulation of lipid droplets in the cytoplasm, and nuclear fragmentation. The combined administration of testosterone and AA or LA slightly increased sebaceous lipogenesis. In contrast, synthetic PPAR ligands were unable to enhance sebaceous lipogenesis. Interestingly, AA synthesis in human sebocytes was significantly stimulated by the prostaglandins (PG) E2 and Δ15‐J2. On the other hand, PPARγ expression was downregulated by the phytoestrogen genistein. Interestingly, 17β‐estradiol has previously been shown to induce the metabolism of PGD2 to Δ12‐PGJ2, a natural PPARγ ligand. In addition, we found that 17β‐estradiol increases IGF‐I synthesis (+28%) and down‐regulates IGF‐IR expression (−37 to −48%), whereas IGF‐I significantly induces sebaceous lipogenesis. In conclusion, sexual hormones are not directly active but are likely to utilize complex mechanisms, including modified known pro‐inflammatory pathways, to modulate sebocyte differentiation.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>keratinocytes</json:string><json:string>receptor</json:string><json:string>epidermal</json:string><json:string>dermatology</json:string><json:string>follicle</json:string><json:string>calcitriol</json:string><json:string>melatonin</json:string><json:string>melanoma</json:string><json:string>fibroblast</json:string><json:string>estrogen</json:string><json:string>androgen</json:string><json:string>cutaneous</json:string><json:string>oxysterols</json:string><json:string>pomc</json:string><json:string>immunoreactivity</json:string><json:string>munster</json:string><json:string>sebaceous</json:string><json:string>oligonucleotides</json:string><json:string>hair follicle</json:string><json:string>sexual hormones</json:string><json:string>human keratinocytes</json:string><json:string>epidermal keratinocytes</json:string><json:string>acth</json:string><json:string>prurigo nodularis</json:string><json:string>keratinocyte differentiation</json:string><json:string>sebaceous lipogenesis</json:string><json:string>melanoma cell lines</json:string><json:string>sebocyte differentiation</json:string><json:string>cultured keratinocytes</json:string><json:string>epidermis</json:string><json:string>splice variants</json:string><json:string>human hair follicles</json:string><json:string>side effects</json:string><json:string>western blot analysis</json:string><json:string>epidermal differentiation</json:string><json:string>cell biology</json:string><json:string>hdmec membranes</json:string><json:string>normal skin</json:string><json:string>postmenopausal women</json:string><json:string>other hand</json:string><json:string>antisense oligonucleotides</json:string><json:string>calcitriol synthesis</json:string><json:string>such treatment</json:string><json:string>epithelial cells</json:string><json:string>human skin</json:string><json:string>vitamin growth inhibition</json:string><json:string>first time</json:string><json:string>psoriasis vulgaris</json:string><json:string>atopic dermatitis</json:string><json:string>wolfgang tilgen1</json:string><json:string>tumor necrosis</json:string><json:string>cholinergic agonists</json:string><json:string>human epidermis</json:string><json:string>functional significance</json:string><json:string>terminal differentiation</json:string><json:string>biomedical sciences</json:string><json:string>oxidative stress</json:string><json:string>human ache</json:string><json:string>cell growth</json:string><json:string>environmental dermatology</json:string><json:string>wahringer gurtel vienna</json:string><json:string>various studies</json:string><json:string>various cell types</json:string><json:string>various melanoma cell lines</json:string><json:string>real time</json:string><json:string>local synthesis</json:string><json:string>complex mechanisms</json:string><json:string>malignant melanoma</json:string><json:string>campus benjamin franklin</json:string><json:string>important role</json:string><json:string>dresden university</json:string><json:string>carl gustav carus</json:string><json:string>organotypic cultures</json:string><json:string>androgen activity</json:string><json:string>vanilloid receptor subtype</json:string><json:string>foreskin keratinocytes</json:string><json:string>recovery time</json:string><json:string>clinical monitoring</json:string><json:string>epidermal hydration</json:string><json:string>skin surface lipids</json:string><json:string>melanocortin receptors</json:string><json:string>ludwig boltzmann institute</json:string><json:string>collagen synthesis</json:string><json:string>dermal papilla cells</json:string><json:string>connective tissue sheath fibroblasts</json:string><json:string>wound healing</json:string><json:string>narrowband lamp</json:string><json:string>hair follicle biology</json:string><json:string>mammalian skin</json:string><json:string>radical scavenger</json:string><json:string>murine hair follicles</json:string><json:string>hair cycle dependence</json:string><json:string>basal serum levels</json:string><json:string>local production</json:string><json:string>melanoma cells</json:string><json:string>pomc peptides</json:string><json:string>dermal microvascular</json:string><json:string>extracellular matrix</json:string><json:string>inhibitor</json:string></teeft></keywords><author><json:item><name>ChC Zouboulis</name><affiliations><json:string>Department of Dermatology, Campus Benjamin Franklin, Charité– Universitaetsmedizin Berlin, Berlin, and §Eicosanoids and Epithelial Tumor Development Research Group, Deutsches Krebsforschungszentrum, Heidelberg, Germany, and *Department of Dermatology, Chang Gung University, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan</json:string></affiliations></json:item><json:item><name>W. Chen</name><affiliations><json:string>Department of Dermatology, Campus Benjamin Franklin, Charité– Universitaetsmedizin Berlin, Berlin, and §Eicosanoids and Epithelial Tumor Development Research Group, Deutsches Krebsforschungszentrum, Heidelberg, Germany, and *Department of Dermatology, Chang Gung University, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan</json:string></affiliations></json:item><json:item><name>Th. Alestas</name><affiliations><json:string>Department of Dermatology, Campus Benjamin Franklin, Charité– Universitaetsmedizin Berlin, Berlin, and §Eicosanoids and Epithelial Tumor Development Research Group, Deutsches Krebsforschungszentrum, Heidelberg, Germany, and *Department of Dermatology, Chang Gung University, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan</json:string></affiliations></json:item><json:item><name>E Makrantonaki</name><affiliations><json:string>Department of Dermatology, Campus Benjamin Franklin, Charité– Universitaetsmedizin Berlin, Berlin, and §Eicosanoids and Epithelial Tumor Development Research Group, Deutsches Krebsforschungszentrum, Heidelberg, Germany, and *Department of Dermatology, Chang Gung University, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan</json:string></affiliations></json:item><json:item><name>H. Seltmann</name><affiliations><json:string>Department of Dermatology, Campus Benjamin Franklin, Charité– Universitaetsmedizin Berlin, Berlin, and §Eicosanoids and Epithelial Tumor Development Research Group, Deutsches Krebsforschungszentrum, Heidelberg, Germany, and *Department of Dermatology, Chang Gung University, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan</json:string></affiliations></json:item><json:item><name>K Müller‐Decker</name><affiliations><json:string>Department of Dermatology, Campus Benjamin Franklin, Charité– Universitaetsmedizin Berlin, Berlin, and §Eicosanoids and Epithelial Tumor Development Research Group, Deutsches Krebsforschungszentrum, Heidelberg, Germany, and *Department of Dermatology, Chang Gung University, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan</json:string></affiliations></json:item></author><articleId><json:string>EXD266L</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>abstract</json:string></originalGenre><abstract>Sexual hormones are important in the maintenance of human skin. Being the endocrine “brain” of the skin, the sebaceous gland is a major target of sexual hormones. While androgens stimulate sebocyte proliferation, estrogens do not to affect sebaceous gland growth. Regarding differentiation, androgens are expected to stimulate and estrogens to suppress sebaceous lipid synthesis, while estrogens, in vivo, enhance sebaceous lipogenesis in aged skin. The latter results have been disputed by current in vitro data indicating no direct effect of sexual hormones on sebocyte differentiation. To elucidate these contradictions we have investigated possible pathways which may be used by sexual hormones to modulate sebocyte differentiation in vitro. It has been postulated that androgen induction of lipogenesis requires the concomitant presence of peroxisome proliferator‐activated receptor (PPAR) ligands. We found that arachidonic acid (AA), the direct precursor of leukotriene B4, a natural PPARα ligand, and linoleic acid (LA), a natural PPARδ ligand, induce sebocyte enlargement, accumulation of lipid droplets in the cytoplasm, and nuclear fragmentation. The combined administration of testosterone and AA or LA slightly increased sebaceous lipogenesis. In contrast, synthetic PPAR ligands were unable to enhance sebaceous lipogenesis. Interestingly, AA synthesis in human sebocytes was significantly stimulated by the prostaglandins (PG) E2 and Δ15‐J2. On the other hand, PPARγ expression was downregulated by the phytoestrogen genistein. Interestingly, 17β‐estradiol has previously been shown to induce the metabolism of PGD2 to Δ12‐PGJ2, a natural PPARγ ligand. In addition, we found that 17β‐estradiol increases IGF‐I synthesis (+28%) and down‐regulates IGF‐IR expression (−37 to −48%), whereas IGF‐I significantly induces sebaceous lipogenesis. In conclusion, sexual hormones are not directly active but are likely to utilize complex mechanisms, including modified known pro‐inflammatory pathways, to modulate sebocyte differentiation.</abstract><qualityIndicators><score>8.5</score><pdfVersion>1.4</pdfVersion><pdfPageSize>595 x 782 pts</pdfPageSize><refBibsNative>false</refBibsNative><abstractCharCount>2043</abstractCharCount><pdfWordCount>5614</pdfWordCount><pdfCharCount>38663</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>280</abstractWordCount></qualityIndicators><title>Sexual hormones utilize complex mechanisms to modulate sebocyte differentiation</title><genre><json:string>abstract</json:string></genre><host><title>Experimental Dermatology</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1600-0625</json:string></doi><issn><json:string>0906-6705</json:string></issn><eissn><json:string>1600-0625</json:string></eissn><publisherId><json:string>EXD</json:string></publisherId><volume>14</volume><issue>2</issue><pages><first>156</first><last>156</last><total>1</total></pages><genre><json:string>journal</json:string></genre></host><categories><wos><json:string>science</json:string><json:string>dermatology</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>dermatology & venereal diseases</json:string></scienceMetrix><inist><json:string>sciences appliquees, technologies et medecines</json:string><json:string>sciences biologiques et medicales</json:string><json:string>sciences medicales</json:string></inist></categories><publicationDate>2005</publicationDate><copyrightDate>2005</copyrightDate><doi><json:string>10.1111/j.0906-6705.2005.0266l.x</json:string></doi><id>EF0FB3B9BE0DC5E158A7FFE0036F3D7951685A9E</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/EF0FB3B9BE0DC5E158A7FFE0036F3D7951685A9E/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/EF0FB3B9BE0DC5E158A7FFE0036F3D7951685A9E/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/EF0FB3B9BE0DC5E158A7FFE0036F3D7951685A9E/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Sexual hormones utilize complex mechanisms to modulate sebocyte differentiation</title><respStmt><resp>Références bibliographiques récupérées via GROBID</resp><name resp="ISTEX-API">ISTEX-API (INIST-CNRS)</name></respStmt><respStmt><resp>Références bibliographiques récupérées via GROBID</resp><name resp="ISTEX-API">ISTEX-API (INIST-CNRS)</name></respStmt></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Munksgaard International Publishers</publisher><pubPlace>Oxford, UK; Malden, USA</pubPlace><availability><p>WILEY</p></availability><date>2005</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Sexual hormones utilize complex mechanisms to modulate sebocyte differentiation</title><author xml:id="author-1"><persName><forename type="first">ChC</forename><surname>Zouboulis</surname></persName><affiliation>Department of Dermatology, Campus Benjamin Franklin, Charité– Universitaetsmedizin Berlin, Berlin, and §Eicosanoids and Epithelial Tumor Development Research Group, Deutsches Krebsforschungszentrum, Heidelberg, Germany, and *Department of Dermatology, Chang Gung University, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan</affiliation></author><author xml:id="author-2"><persName><forename type="first">W.</forename><surname>Chen</surname></persName><affiliation>Department of Dermatology, Campus Benjamin Franklin, Charité– Universitaetsmedizin Berlin, Berlin, and §Eicosanoids and Epithelial Tumor Development Research Group, Deutsches Krebsforschungszentrum, Heidelberg, Germany, and *Department of Dermatology, Chang Gung University, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan</affiliation></author><author xml:id="author-3"><persName><forename type="first">Th.</forename><surname>Alestas</surname></persName><affiliation>Department of Dermatology, Campus Benjamin Franklin, Charité– Universitaetsmedizin Berlin, Berlin, and §Eicosanoids and Epithelial Tumor Development Research Group, Deutsches Krebsforschungszentrum, Heidelberg, Germany, and *Department of Dermatology, Chang Gung University, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan</affiliation></author><author xml:id="author-4"><persName><forename type="first">E</forename><surname>Makrantonaki</surname></persName><affiliation>Department of Dermatology, Campus Benjamin Franklin, Charité– Universitaetsmedizin Berlin, Berlin, and §Eicosanoids and Epithelial Tumor Development Research Group, Deutsches Krebsforschungszentrum, Heidelberg, Germany, and *Department of Dermatology, Chang Gung University, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan</affiliation></author><author xml:id="author-5"><persName><forename type="first">H.</forename><surname>Seltmann</surname></persName><affiliation>Department of Dermatology, Campus Benjamin Franklin, Charité– Universitaetsmedizin Berlin, Berlin, and §Eicosanoids and Epithelial Tumor Development Research Group, Deutsches Krebsforschungszentrum, Heidelberg, Germany, and *Department of Dermatology, Chang Gung University, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan</affiliation></author><author xml:id="author-6"><persName><forename type="first">K</forename><surname>Müller‐Decker</surname></persName><affiliation>Department of Dermatology, Campus Benjamin Franklin, Charité– Universitaetsmedizin Berlin, Berlin, and §Eicosanoids and Epithelial Tumor Development Research Group, Deutsches Krebsforschungszentrum, Heidelberg, Germany, and *Department of Dermatology, Chang Gung University, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan</affiliation></author></analytic><monogr><title level="j">Experimental Dermatology</title><idno type="pISSN">0906-6705</idno><idno type="eISSN">1600-0625</idno><idno type="DOI">10.1111/(ISSN)1600-0625</idno><imprint><publisher>Munksgaard International Publishers</publisher><pubPlace>Oxford, UK; Malden, USA</pubPlace><date type="published" when="2005-02"></date><biblScope unit="volume">14</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="156">156</biblScope><biblScope unit="page" to="156">156</biblScope></imprint></monogr><idno type="istex">EF0FB3B9BE0DC5E158A7FFE0036F3D7951685A9E</idno><idno type="DOI">10.1111/j.0906-6705.2005.0266l.x</idno><idno type="ArticleID">EXD266L</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2005</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Sexual hormones are important in the maintenance of human skin. Being the endocrine “brain” of the skin, the sebaceous gland is a major target of sexual hormones. While androgens stimulate sebocyte proliferation, estrogens do not to affect sebaceous gland growth. Regarding differentiation, androgens are expected to stimulate and estrogens to suppress sebaceous lipid synthesis, while estrogens, in vivo, enhance sebaceous lipogenesis in aged skin. The latter results have been disputed by current in vitro data indicating no direct effect of sexual hormones on sebocyte differentiation. To elucidate these contradictions we have investigated possible pathways which may be used by sexual hormones to modulate sebocyte differentiation in vitro. It has been postulated that androgen induction of lipogenesis requires the concomitant presence of peroxisome proliferator‐activated receptor (PPAR) ligands. We found that arachidonic acid (AA), the direct precursor of leukotriene B4, a natural PPARα ligand, and linoleic acid (LA), a natural PPARδ ligand, induce sebocyte enlargement, accumulation of lipid droplets in the cytoplasm, and nuclear fragmentation. The combined administration of testosterone and AA or LA slightly increased sebaceous lipogenesis. In contrast, synthetic PPAR ligands were unable to enhance sebaceous lipogenesis. Interestingly, AA synthesis in human sebocytes was significantly stimulated by the prostaglandins (PG) E2 and Δ15‐J2. On the other hand, PPARγ expression was downregulated by the phytoestrogen genistein. Interestingly, 17β‐estradiol has previously been shown to induce the metabolism of PGD2 to Δ12‐PGJ2, a natural PPARγ ligand. In addition, we found that 17β‐estradiol increases IGF‐I synthesis (+28%) and down‐regulates IGF‐IR expression (−37 to −48%), whereas IGF‐I significantly induces sebaceous lipogenesis. In conclusion, sexual hormones are not directly active but are likely to utilize complex mechanisms, including modified known pro‐inflammatory pathways, to modulate sebocyte differentiation.</p></abstract></profileDesc><revisionDesc><change when="2005-02">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-12-12">References added</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2017-02-8">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/EF0FB3B9BE0DC5E158A7FFE0036F3D7951685A9E/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley component found"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Munksgaard International Publishers</publisherName><publisherLoc>Oxford, UK; 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Being the endocrine “brain” of the skin, the sebaceous gland is a major target of sexual hormones. While androgens stimulate sebocyte proliferation, estrogens do not to affect sebaceous gland growth. Regarding differentiation, androgens are expected to stimulate and estrogens to suppress sebaceous lipid synthesis, while estrogens, <i>in vivo</i>, enhance sebaceous lipogenesis in aged skin. The latter results have been disputed by current <i>in vitro</i> data indicating no direct effect of sexual hormones on sebocyte differentiation. To elucidate these contradictions we have investigated possible pathways which may be used by sexual hormones to modulate sebocyte differentiation in vitro. It has been postulated that androgen induction of lipogenesis requires the concomitant presence of peroxisome proliferator‐activated receptor (PPAR) ligands. We found that arachidonic acid (AA), the direct precursor of leukotriene B4, a natural PPARα ligand, and linoleic acid (LA), a natural PPARδ ligand, induce sebocyte enlargement, accumulation of lipid droplets in the cytoplasm, and nuclear fragmentation. The combined administration of testosterone and AA or LA slightly increased sebaceous lipogenesis. In contrast, synthetic PPAR ligands were unable to enhance sebaceous lipogenesis. Interestingly, AA synthesis in human sebocytes was significantly stimulated by the prostaglandins (PG) E2 and Δ15‐J2. On the other hand, PPARγ expression was downregulated by the phytoestrogen genistein. Interestingly, 17β‐estradiol has previously been shown to induce the metabolism of PGD2 to Δ12‐PGJ2, a natural PPARγ ligand. In addition, we found that 17β‐estradiol increases IGF‐I synthesis (+28%) and down‐regulates IGF‐IR expression (−37 to −48%), whereas IGF‐I significantly induces sebaceous lipogenesis. In conclusion, sexual hormones are not directly active but are likely to utilize complex mechanisms, including modified known pro‐inflammatory pathways, to modulate sebocyte differentiation.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Sexual hormones utilize complex mechanisms to modulate sebocyte differentiation</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Abstracts</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Sexual hormones utilize complex mechanisms to modulate sebocyte differentiation</title></titleInfo><name type="personal"><namePart type="given">ChC</namePart><namePart type="family">Zouboulis</namePart><affiliation>Department of Dermatology, Campus Benjamin Franklin, Charité– Universitaetsmedizin Berlin, Berlin, and §Eicosanoids and Epithelial Tumor Development Research Group, Deutsches Krebsforschungszentrum, Heidelberg, Germany, and *Department of Dermatology, Chang Gung University, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W.</namePart><namePart type="family">Chen</namePart><affiliation>Department of Dermatology, Campus Benjamin Franklin, Charité– Universitaetsmedizin Berlin, Berlin, and §Eicosanoids and Epithelial Tumor Development Research Group, Deutsches Krebsforschungszentrum, Heidelberg, Germany, and *Department of Dermatology, Chang Gung University, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Th.</namePart><namePart type="family">Alestas</namePart><affiliation>Department of Dermatology, Campus Benjamin Franklin, Charité– Universitaetsmedizin Berlin, Berlin, and §Eicosanoids and Epithelial Tumor Development Research Group, Deutsches Krebsforschungszentrum, Heidelberg, Germany, and *Department of Dermatology, Chang Gung University, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E</namePart><namePart type="family">Makrantonaki</namePart><affiliation>Department of Dermatology, Campus Benjamin Franklin, Charité– Universitaetsmedizin Berlin, Berlin, and §Eicosanoids and Epithelial Tumor Development Research Group, Deutsches Krebsforschungszentrum, Heidelberg, Germany, and *Department of Dermatology, Chang Gung University, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">Seltmann</namePart><affiliation>Department of Dermatology, Campus Benjamin Franklin, Charité– Universitaetsmedizin Berlin, Berlin, and §Eicosanoids and Epithelial Tumor Development Research Group, Deutsches Krebsforschungszentrum, Heidelberg, Germany, and *Department of Dermatology, Chang Gung University, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Müller‐Decker</namePart><affiliation>Department of Dermatology, Campus Benjamin Franklin, Charité– Universitaetsmedizin Berlin, Berlin, and §Eicosanoids and Epithelial Tumor Development Research Group, Deutsches Krebsforschungszentrum, Heidelberg, Germany, and *Department of Dermatology, Chang Gung University, Chang Gung Memorial Hospital Kaohsiung, Kaohsiung, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="abstract" displayLabel="abstract"></genre><originInfo><publisher>Munksgaard International Publishers</publisher><place><placeTerm type="text">Oxford, UK; Malden, USA</placeTerm></place><dateIssued encoding="w3cdtf">2005-02</dateIssued><copyrightDate encoding="w3cdtf">2005</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Sexual hormones are important in the maintenance of human skin. Being the endocrine “brain” of the skin, the sebaceous gland is a major target of sexual hormones. While androgens stimulate sebocyte proliferation, estrogens do not to affect sebaceous gland growth. Regarding differentiation, androgens are expected to stimulate and estrogens to suppress sebaceous lipid synthesis, while estrogens, in vivo, enhance sebaceous lipogenesis in aged skin. The latter results have been disputed by current in vitro data indicating no direct effect of sexual hormones on sebocyte differentiation. To elucidate these contradictions we have investigated possible pathways which may be used by sexual hormones to modulate sebocyte differentiation in vitro. It has been postulated that androgen induction of lipogenesis requires the concomitant presence of peroxisome proliferator‐activated receptor (PPAR) ligands. We found that arachidonic acid (AA), the direct precursor of leukotriene B4, a natural PPARα ligand, and linoleic acid (LA), a natural PPARδ ligand, induce sebocyte enlargement, accumulation of lipid droplets in the cytoplasm, and nuclear fragmentation. The combined administration of testosterone and AA or LA slightly increased sebaceous lipogenesis. In contrast, synthetic PPAR ligands were unable to enhance sebaceous lipogenesis. Interestingly, AA synthesis in human sebocytes was significantly stimulated by the prostaglandins (PG) E2 and Δ15‐J2. On the other hand, PPARγ expression was downregulated by the phytoestrogen genistein. Interestingly, 17β‐estradiol has previously been shown to induce the metabolism of PGD2 to Δ12‐PGJ2, a natural PPARγ ligand. In addition, we found that 17β‐estradiol increases IGF‐I synthesis (+28%) and down‐regulates IGF‐IR expression (−37 to −48%), whereas IGF‐I significantly induces sebaceous lipogenesis. In conclusion, sexual hormones are not directly active but are likely to utilize complex mechanisms, including modified known pro‐inflammatory pathways, to modulate sebocyte differentiation.</abstract><relatedItem type="host"><titleInfo><title>Experimental Dermatology</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0906-6705</identifier><identifier type="eISSN">1600-0625</identifier><identifier type="DOI">10.1111/(ISSN)1600-0625</identifier><identifier type="PublisherID">EXD</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>14</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>156</start><end>156</end><total>1</total></extent></part></relatedItem><identifier type="istex">EF0FB3B9BE0DC5E158A7FFE0036F3D7951685A9E</identifier><identifier type="DOI">10.1111/j.0906-6705.2005.0266l.x</identifier><identifier type="ArticleID">EXD266L</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Munksgaard International Publishers</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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