Stimulation of keratinocyte differentiation – a new role for the vanilloid receptor subtype 1 (VR1/TRPV1)?
Identifieur interne : 000992 ( Istex/Corpus ); précédent : 000991; suivant : 000993Stimulation of keratinocyte differentiation – a new role for the vanilloid receptor subtype 1 (VR1/TRPV1)?
Auteurs : Sonja St Nder ; Corinna Moormann ; Mark Schumacher ; Dieter Metze ; Thomas A. Luger ; Martin SteinhoffSource :
- 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
Vanilloids and endogenous cannabinoids mediate their actions via the vanilloid receptor subtype 1 (VR1/TRPV1), a non‐selective cation channel, which is widely distributed in the central and peripheral nervous system. Only recently, VR1 has been shown to be expressed in keratinocytes in vitro and in vivo. However, a precise description of VR1 localization in epithelial cells was missing. To determine this, we investigated VR1‐immunoreactivity as well as mRNA and protein expression in a series of biopsies from normal, diseased, and capsaicin‐treated human skin. VR1 was found in epidermal keratinocytes, the inner root sheet and the infundibulum of hair follicles, differentiated sebocytes, sweat gland ducts, and the secretory portion of eccrine sweat glands upon immunohistochemistry, RT‐PCR and Western blot analysis. Interestingly, in diseased skin such as prurigo nodularis, psoriasis vulgaris, and atopic dermatitis, VR1 expression in keratinocytes correlated with the degree of epidermal differentiation. Enhanced VR1 immunoreactivity and protein content was found in prurigo nodularis in which epidermal keratinocytes are highly differentiated. Under effective capsaicin therapy of prurigo nodularis, the epidermis thinned and the distribution pattern of VR1 on epidermal keratinocytes normalized. In psoriasis vulgaris, a disease with disturbed epidermal differentiation, less intense immunostaining for VR1 was observed. This could be confirmed by western blot analysis showing less VR1 protein amount in comparison to prurigo nodularis although histologically both showed a thickened epidermis. In atopic dermatitis, which is characterized by a moderate epidermal hyperplasia only and regular differentiated keratinocytes, VR1 immunoreactivity was unchanged in comparison to normal skin. These findings suggest that VR1 may contribute to regular differentiation of keratinocytes. VR1 activation opens non‐selective cation channels with high permeability to calcium, a ion that is crucially important for the synthesis of cornification proteins such as involucrin, fillagrin and loricrin. The role of VR1 in other epithelial cells of appendage structures remains to be determined. In summary, VR1 is widely distributed in the skin suggesting a central role for this receptor not only in nociception but also maturation and function of epithelial cells.
Url:
DOI: 10.1111/j.0906-6705.2005.0266h.x
Links to Exploration step
ISTEX:5D85247B9BA9303E193C6DFDD2B843FF0F739EEBLe document en format XML
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Luger</name><affiliation><mods:affiliation>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</mods:affiliation></affiliation></author><author><name sortKey="Steinhoff, Martin" sort="Steinhoff, Martin" uniqKey="Steinhoff M" first="Martin" last="Steinhoff">Martin Steinhoff</name><affiliation><mods:affiliation>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</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="155">155</biblScope><biblScope unit="page" to="155">155</biblScope></imprint><idno type="ISSN">0906-6705</idno></series><idno type="istex">5D85247B9BA9303E193C6DFDD2B843FF0F739EEB</idno><idno type="DOI">10.1111/j.0906-6705.2005.0266h.x</idno><idno type="ArticleID">EXD266H</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">Vanilloids and endogenous cannabinoids mediate their actions via the vanilloid receptor subtype 1 (VR1/TRPV1), a non‐selective cation channel, which is widely distributed in the central and peripheral nervous system. Only recently, VR1 has been shown to be expressed in keratinocytes in vitro and in vivo. However, a precise description of VR1 localization in epithelial cells was missing. To determine this, we investigated VR1‐immunoreactivity as well as mRNA and protein expression in a series of biopsies from normal, diseased, and capsaicin‐treated human skin. VR1 was found in epidermal keratinocytes, the inner root sheet and the infundibulum of hair follicles, differentiated sebocytes, sweat gland ducts, and the secretory portion of eccrine sweat glands upon immunohistochemistry, RT‐PCR and Western blot analysis. Interestingly, in diseased skin such as prurigo nodularis, psoriasis vulgaris, and atopic dermatitis, VR1 expression in keratinocytes correlated with the degree of epidermal differentiation. Enhanced VR1 immunoreactivity and protein content was found in prurigo nodularis in which epidermal keratinocytes are highly differentiated. Under effective capsaicin therapy of prurigo nodularis, the epidermis thinned and the distribution pattern of VR1 on epidermal keratinocytes normalized. In psoriasis vulgaris, a disease with disturbed epidermal differentiation, less intense immunostaining for VR1 was observed. This could be confirmed by western blot analysis showing less VR1 protein amount in comparison to prurigo nodularis although histologically both showed a thickened epidermis. In atopic dermatitis, which is characterized by a moderate epidermal hyperplasia only and regular differentiated keratinocytes, VR1 immunoreactivity was unchanged in comparison to normal skin. These findings suggest that VR1 may contribute to regular differentiation of keratinocytes. VR1 activation opens non‐selective cation channels with high permeability to calcium, a ion that is crucially important for the synthesis of cornification proteins such as involucrin, fillagrin and loricrin. The role of VR1 in other epithelial cells of appendage structures remains to be determined. In summary, VR1 is widely distributed in the skin suggesting a central role for this receptor not only in nociception but also maturation and function of epithelial cells.</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>Sonja Ständer</name><affiliations><json:string>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</json:string></affiliations></json:item><json:item><name>Corinna Moormann</name><affiliations><json:string>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</json:string></affiliations></json:item><json:item><name>Mark Schumacher</name><affiliations><json:string>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</json:string></affiliations></json:item><json:item><name>Dieter Metze</name><affiliations><json:string>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</json:string></affiliations></json:item><json:item><name>Thomas A. Luger</name><affiliations><json:string>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</json:string></affiliations></json:item><json:item><name>Martin Steinhoff</name><affiliations><json:string>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</json:string></affiliations></json:item></author><articleId><json:string>EXD266H</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>abstract</json:string></originalGenre><abstract>Vanilloids and endogenous cannabinoids mediate their actions via the vanilloid receptor subtype 1 (VR1/TRPV1), a non‐selective cation channel, which is widely distributed in the central and peripheral nervous system. Only recently, VR1 has been shown to be expressed in keratinocytes in vitro and in vivo. However, a precise description of VR1 localization in epithelial cells was missing. To determine this, we investigated VR1‐immunoreactivity as well as mRNA and protein expression in a series of biopsies from normal, diseased, and capsaicin‐treated human skin. VR1 was found in epidermal keratinocytes, the inner root sheet and the infundibulum of hair follicles, differentiated sebocytes, sweat gland ducts, and the secretory portion of eccrine sweat glands upon immunohistochemistry, RT‐PCR and Western blot analysis. Interestingly, in diseased skin such as prurigo nodularis, psoriasis vulgaris, and atopic dermatitis, VR1 expression in keratinocytes correlated with the degree of epidermal differentiation. Enhanced VR1 immunoreactivity and protein content was found in prurigo nodularis in which epidermal keratinocytes are highly differentiated. Under effective capsaicin therapy of prurigo nodularis, the epidermis thinned and the distribution pattern of VR1 on epidermal keratinocytes normalized. In psoriasis vulgaris, a disease with disturbed epidermal differentiation, less intense immunostaining for VR1 was observed. This could be confirmed by western blot analysis showing less VR1 protein amount in comparison to prurigo nodularis although histologically both showed a thickened epidermis. In atopic dermatitis, which is characterized by a moderate epidermal hyperplasia only and regular differentiated keratinocytes, VR1 immunoreactivity was unchanged in comparison to normal skin. These findings suggest that VR1 may contribute to regular differentiation of keratinocytes. VR1 activation opens non‐selective cation channels with high permeability to calcium, a ion that is crucially important for the synthesis of cornification proteins such as involucrin, fillagrin and loricrin. The role of VR1 in other epithelial cells of appendage structures remains to be determined. 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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">Stimulation of keratinocyte differentiation – a new role for the vanilloid receptor subtype 1 (VR1/TRPV1)?</title><author xml:id="author-1"><persName><forename type="first">Sonja</forename><surname>Ständer</surname></persName><affiliation>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</affiliation></author><author xml:id="author-2"><persName><forename type="first">Corinna</forename><surname>Moormann</surname></persName><affiliation>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</affiliation></author><author xml:id="author-3"><persName><forename type="first">Mark</forename><surname>Schumacher</surname></persName><affiliation>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</affiliation></author><author xml:id="author-4"><persName><forename type="first">Dieter</forename><surname>Metze</surname></persName><affiliation>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</affiliation></author><author xml:id="author-5"><persName><forename type="first">Thomas A.</forename><surname>Luger</surname></persName><affiliation>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</affiliation></author><author xml:id="author-6"><persName><forename type="first">Martin</forename><surname>Steinhoff</surname></persName><affiliation>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</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="155">155</biblScope><biblScope unit="page" to="155">155</biblScope></imprint></monogr><idno type="istex">5D85247B9BA9303E193C6DFDD2B843FF0F739EEB</idno><idno type="DOI">10.1111/j.0906-6705.2005.0266h.x</idno><idno type="ArticleID">EXD266H</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2005</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Vanilloids and endogenous cannabinoids mediate their actions via the vanilloid receptor subtype 1 (VR1/TRPV1), a non‐selective cation channel, which is widely distributed in the central and peripheral nervous system. Only recently, VR1 has been shown to be expressed in keratinocytes in vitro and in vivo. However, a precise description of VR1 localization in epithelial cells was missing. To determine this, we investigated VR1‐immunoreactivity as well as mRNA and protein expression in a series of biopsies from normal, diseased, and capsaicin‐treated human skin. VR1 was found in epidermal keratinocytes, the inner root sheet and the infundibulum of hair follicles, differentiated sebocytes, sweat gland ducts, and the secretory portion of eccrine sweat glands upon immunohistochemistry, RT‐PCR and Western blot analysis. Interestingly, in diseased skin such as prurigo nodularis, psoriasis vulgaris, and atopic dermatitis, VR1 expression in keratinocytes correlated with the degree of epidermal differentiation. Enhanced VR1 immunoreactivity and protein content was found in prurigo nodularis in which epidermal keratinocytes are highly differentiated. Under effective capsaicin therapy of prurigo nodularis, the epidermis thinned and the distribution pattern of VR1 on epidermal keratinocytes normalized. In psoriasis vulgaris, a disease with disturbed epidermal differentiation, less intense immunostaining for VR1 was observed. This could be confirmed by western blot analysis showing less VR1 protein amount in comparison to prurigo nodularis although histologically both showed a thickened epidermis. In atopic dermatitis, which is characterized by a moderate epidermal hyperplasia only and regular differentiated keratinocytes, VR1 immunoreactivity was unchanged in comparison to normal skin. These findings suggest that VR1 may contribute to regular differentiation of keratinocytes. VR1 activation opens non‐selective cation channels with high permeability to calcium, a ion that is crucially important for the synthesis of cornification proteins such as involucrin, fillagrin and loricrin. The role of VR1 in other epithelial cells of appendage structures remains to be determined. In summary, VR1 is widely distributed in the skin suggesting a central role for this receptor not only in nociception but also maturation and function of epithelial cells.</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/5D85247B9BA9303E193C6DFDD2B843FF0F739EEB/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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Only recently, VR1 has been shown to be expressed in keratinocytes in vitro and in vivo. However, a precise description of VR1 localization in epithelial cells was missing. To determine this, we investigated VR1‐immunoreactivity as well as mRNA and protein expression in a series of biopsies from normal, diseased, and capsaicin‐treated human skin. VR1 was found in epidermal keratinocytes, the inner root sheet and the infundibulum of hair follicles, differentiated sebocytes, sweat gland ducts, and the secretory portion of eccrine sweat glands upon immunohistochemistry, RT‐PCR and Western blot analysis. Interestingly, in diseased skin such as prurigo nodularis, psoriasis vulgaris, and atopic dermatitis, VR1 expression in keratinocytes correlated with the degree of epidermal differentiation. Enhanced VR1 immunoreactivity and protein content was found in prurigo nodularis in which epidermal keratinocytes are highly differentiated. Under effective capsaicin therapy of prurigo nodularis, the epidermis thinned and the distribution pattern of VR1 on epidermal keratinocytes normalized. In psoriasis vulgaris, a disease with disturbed epidermal differentiation, less intense immunostaining for VR1 was observed. This could be confirmed by western blot analysis showing less VR1 protein amount in comparison to prurigo nodularis although histologically both showed a thickened epidermis. In atopic dermatitis, which is characterized by a moderate epidermal hyperplasia only and regular differentiated keratinocytes, VR1 immunoreactivity was unchanged in comparison to normal skin. These findings suggest that VR1 may contribute to regular differentiation of keratinocytes. VR1 activation opens non‐selective cation channels with high permeability to calcium, a ion that is crucially important for the synthesis of cornification proteins such as involucrin, fillagrin and loricrin. The role of VR1 in other epithelial cells of appendage structures remains to be determined. In summary, VR1 is widely distributed in the skin suggesting a central role for this receptor not only in nociception but also maturation and function of epithelial cells.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Stimulation of keratinocyte differentiation – a new role for the vanilloid receptor subtype 1 (VR1/TRPV1)?</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Abstracts</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Stimulation of keratinocyte differentiation – a new role for the vanilloid receptor subtype 1 (VR1/TRPV1)?</title></titleInfo><name type="personal"><namePart type="given">Sonja</namePart><namePart type="family">Ständer</namePart><affiliation>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Corinna</namePart><namePart type="family">Moormann</namePart><affiliation>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mark</namePart><namePart type="family">Schumacher</namePart><affiliation>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Dieter</namePart><namePart type="family">Metze</namePart><affiliation>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thomas A.</namePart><namePart type="family">Luger</namePart><affiliation>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Martin</namePart><namePart type="family">Steinhoff</namePart><affiliation>1 Department of Dermatology and 2 Ludwig Boltzmann Institute for Cell Biology and Immunobiology of the Skin, University of Münster, Münster, Germany, 3 Department of Anesthesia and Postoperative Care, University of California, San Francisco, USA</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">Vanilloids and endogenous cannabinoids mediate their actions via the vanilloid receptor subtype 1 (VR1/TRPV1), a non‐selective cation channel, which is widely distributed in the central and peripheral nervous system. Only recently, VR1 has been shown to be expressed in keratinocytes in vitro and in vivo. However, a precise description of VR1 localization in epithelial cells was missing. To determine this, we investigated VR1‐immunoreactivity as well as mRNA and protein expression in a series of biopsies from normal, diseased, and capsaicin‐treated human skin. VR1 was found in epidermal keratinocytes, the inner root sheet and the infundibulum of hair follicles, differentiated sebocytes, sweat gland ducts, and the secretory portion of eccrine sweat glands upon immunohistochemistry, RT‐PCR and Western blot analysis. Interestingly, in diseased skin such as prurigo nodularis, psoriasis vulgaris, and atopic dermatitis, VR1 expression in keratinocytes correlated with the degree of epidermal differentiation. Enhanced VR1 immunoreactivity and protein content was found in prurigo nodularis in which epidermal keratinocytes are highly differentiated. Under effective capsaicin therapy of prurigo nodularis, the epidermis thinned and the distribution pattern of VR1 on epidermal keratinocytes normalized. In psoriasis vulgaris, a disease with disturbed epidermal differentiation, less intense immunostaining for VR1 was observed. This could be confirmed by western blot analysis showing less VR1 protein amount in comparison to prurigo nodularis although histologically both showed a thickened epidermis. In atopic dermatitis, which is characterized by a moderate epidermal hyperplasia only and regular differentiated keratinocytes, VR1 immunoreactivity was unchanged in comparison to normal skin. These findings suggest that VR1 may contribute to regular differentiation of keratinocytes. VR1 activation opens non‐selective cation channels with high permeability to calcium, a ion that is crucially important for the synthesis of cornification proteins such as involucrin, fillagrin and loricrin. The role of VR1 in other epithelial cells of appendage structures remains to be determined. In summary, VR1 is widely distributed in the skin suggesting a central role for this receptor not only in nociception but also maturation and function of epithelial cells.</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>155</start><end>155</end><total>1</total></extent></part></relatedItem><identifier type="istex">5D85247B9BA9303E193C6DFDD2B843FF0F739EEB</identifier><identifier type="DOI">10.1111/j.0906-6705.2005.0266h.x</identifier><identifier type="ArticleID">EXD266H</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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