Glucocorticoid receptors GRα and GRβ are expressed in inflammatory dermatoses
Background Glucocorticoids (GC) are the most commonly used antiinflammatory drugs in dermatology. The actions of GCs are mediated by the glucocorticoid receptor (GR). Alternative splicing of GR mRNA gives rise to different isoforms, GRα and GRβ being the most important. GRβ antagonizes the activity...
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| Veröffentlicht in: | EJD. European journal of dermatology 2016, Vol.26 (1), p.21-27 |
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| creator | Kubin, Minna E. Hägg, Päivi M. Kokkonen, Nina Väyrynen, Juha P. Haapasaari, Kirsi-Maria Moilanen, Jyri Kallioinen, Matti Hurskainen, Tiina Tasanen, Kaisa |
| description | Background
Glucocorticoids (GC) are the most commonly used antiinflammatory drugs in dermatology. The actions of GCs are mediated by the glucocorticoid receptor (GR). Alternative splicing of GR mRNA gives rise to different isoforms, GRα and GRβ being the most important. GRβ antagonizes the activity of GRα and its up-regulation has been associated with glucocorticoid insensitivity in several non-cutaneous inflammatory diseases.
Methods
Using immunohistochemical stainings, we analyzed the expression of GRα and GRβ in lesional skin samples of patients with atopic dermatitis, lichen ruber planus, eczema nummulare and lichen simplex chronicus.We also conducted a study of 13 severe atopic patients to investigate the effect of prednisolone treatment on the expression of GR isoforms using quantitative PCR, western blot and immunohistochemical analysis.
Results
GRα and GRβ were expressed in atopic dermatitis, lichen ruber planus, eczema nummulare and lichen simplex chronicus. Our novel finding was that GRα is abundant in keratinocytes and cutaneous neutrophils. Nuclear staining of both GRα and GRβ was strongest in keratinocytes of patients with lichen ruber planus, whereas the least nuclear positivity was detected in keratinocytes of patients with atopic dermatitis. In severe atopic dermatitis GRα and GRβ were expressed in both peripheral blood mononuclear cells and the skin. The expression of GRα and GRβ varied during prednisolone therapy but the changes were not related to treatment response or GC insensitivity.
Conclusion
GRα and GRβ are expressed in inflammatory dermatoses. In severe atopic dermatitis the increased expression of GRβ mRNA is not connected to insensitivity against prednisolone treatment. |
| doi_str_mv | 10.1684/ejd.2015.2691 |
| format | Article |
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Glucocorticoids (GC) are the most commonly used antiinflammatory drugs in dermatology. The actions of GCs are mediated by the glucocorticoid receptor (GR). Alternative splicing of GR mRNA gives rise to different isoforms, GRα and GRβ being the most important. GRβ antagonizes the activity of GRα and its up-regulation has been associated with glucocorticoid insensitivity in several non-cutaneous inflammatory diseases.
Methods
Using immunohistochemical stainings, we analyzed the expression of GRα and GRβ in lesional skin samples of patients with atopic dermatitis, lichen ruber planus, eczema nummulare and lichen simplex chronicus.We also conducted a study of 13 severe atopic patients to investigate the effect of prednisolone treatment on the expression of GR isoforms using quantitative PCR, western blot and immunohistochemical analysis.
Results
GRα and GRβ were expressed in atopic dermatitis, lichen ruber planus, eczema nummulare and lichen simplex chronicus. Our novel finding was that GRα is abundant in keratinocytes and cutaneous neutrophils. Nuclear staining of both GRα and GRβ was strongest in keratinocytes of patients with lichen ruber planus, whereas the least nuclear positivity was detected in keratinocytes of patients with atopic dermatitis. In severe atopic dermatitis GRα and GRβ were expressed in both peripheral blood mononuclear cells and the skin. The expression of GRα and GRβ varied during prednisolone therapy but the changes were not related to treatment response or GC insensitivity.
Conclusion
GRα and GRβ are expressed in inflammatory dermatoses. In severe atopic dermatitis the increased expression of GRβ mRNA is not connected to insensitivity against prednisolone treatment.</description><identifier>ISSN: 1167-1122</identifier><identifier>EISSN: 1952-4013</identifier><identifier>DOI: 10.1684/ejd.2015.2691</identifier><identifier>PMID: 26711698</identifier><language>eng</language><publisher>Paris: John Libbey Eurotext</publisher><subject>Adult ; Dermatitis - drug therapy ; Dermatitis - metabolism ; Dermatitis, Atopic - drug therapy ; Dermatitis, Atopic - metabolism ; Dermatology ; Drug Resistance ; Eczema - metabolism ; Female ; Glucocorticoids - therapeutic use ; Humans ; Immunohistochemistry ; Investigative Report ; Keratinocytes - metabolism ; Lichen Planus - metabolism ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Neurodermatitis - metabolism ; Neutrophils - metabolism ; Prednisolone - therapeutic use ; Receptors, Glucocorticoid - metabolism ; RNA, Messenger - metabolism ; Skin - metabolism ; Up-Regulation ; Young Adult</subject><ispartof>EJD. European journal of dermatology, 2016, Vol.26 (1), p.21-27</ispartof><rights>John Libbey Eurotext 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c332t-64655d274c274b145e4251258490e5348b9396d1470bc509f7f2688eb3d1487d3</citedby><cites>FETCH-LOGICAL-c332t-64655d274c274b145e4251258490e5348b9396d1470bc509f7f2688eb3d1487d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1684/ejd.2015.2691$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1684/ejd.2015.2691$$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/26711698$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kubin, Minna E.</creatorcontrib><creatorcontrib>Hägg, Päivi M.</creatorcontrib><creatorcontrib>Kokkonen, Nina</creatorcontrib><creatorcontrib>Väyrynen, Juha P.</creatorcontrib><creatorcontrib>Haapasaari, Kirsi-Maria</creatorcontrib><creatorcontrib>Moilanen, Jyri</creatorcontrib><creatorcontrib>Kallioinen, Matti</creatorcontrib><creatorcontrib>Hurskainen, Tiina</creatorcontrib><creatorcontrib>Tasanen, Kaisa</creatorcontrib><title>Glucocorticoid receptors GRα and GRβ are expressed in inflammatory dermatoses</title><title>EJD. European journal of dermatology</title><addtitle>Eur J Dermatol</addtitle><addtitle>Eur J Dermatol</addtitle><description>Background
Glucocorticoids (GC) are the most commonly used antiinflammatory drugs in dermatology. The actions of GCs are mediated by the glucocorticoid receptor (GR). Alternative splicing of GR mRNA gives rise to different isoforms, GRα and GRβ being the most important. GRβ antagonizes the activity of GRα and its up-regulation has been associated with glucocorticoid insensitivity in several non-cutaneous inflammatory diseases.
Methods
Using immunohistochemical stainings, we analyzed the expression of GRα and GRβ in lesional skin samples of patients with atopic dermatitis, lichen ruber planus, eczema nummulare and lichen simplex chronicus.We also conducted a study of 13 severe atopic patients to investigate the effect of prednisolone treatment on the expression of GR isoforms using quantitative PCR, western blot and immunohistochemical analysis.
Results
GRα and GRβ were expressed in atopic dermatitis, lichen ruber planus, eczema nummulare and lichen simplex chronicus. Our novel finding was that GRα is abundant in keratinocytes and cutaneous neutrophils. Nuclear staining of both GRα and GRβ was strongest in keratinocytes of patients with lichen ruber planus, whereas the least nuclear positivity was detected in keratinocytes of patients with atopic dermatitis. In severe atopic dermatitis GRα and GRβ were expressed in both peripheral blood mononuclear cells and the skin. The expression of GRα and GRβ varied during prednisolone therapy but the changes were not related to treatment response or GC insensitivity.
Conclusion
GRα and GRβ are expressed in inflammatory dermatoses. In severe atopic dermatitis the increased expression of GRβ mRNA is not connected to insensitivity against prednisolone treatment.</description><subject>Adult</subject><subject>Dermatitis - drug therapy</subject><subject>Dermatitis - metabolism</subject><subject>Dermatitis, Atopic - drug therapy</subject><subject>Dermatitis, Atopic - metabolism</subject><subject>Dermatology</subject><subject>Drug Resistance</subject><subject>Eczema - metabolism</subject><subject>Female</subject><subject>Glucocorticoids - therapeutic use</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Investigative Report</subject><subject>Keratinocytes - metabolism</subject><subject>Lichen Planus - metabolism</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Neurodermatitis - metabolism</subject><subject>Neutrophils - metabolism</subject><subject>Prednisolone - therapeutic use</subject><subject>Receptors, Glucocorticoid - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Skin - metabolism</subject><subject>Up-Regulation</subject><subject>Young Adult</subject><issn>1167-1122</issn><issn>1952-4013</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kMtKxDAUhoMojo4u3UqXblpzbZKlDDoKAwOi69Amp9KhN5MpOI-lD-IzmTKjOyEhPzkfP5wPoSuCM5Irfgsbl1FMREZzTY7QGdGCphwTdhwzyWVKCKUzdB7CBmOKNVOnaEZzGWdanaH1shltb3u_rW1fu8SDhWHb-5Asn78_k6JzU_hKCg8JfAweQgCX1F08VVO0bRHZXeLATylAuEAnVdEEuDy8c_T6cP-yeExX6-XT4m6VWsboNs15LoSjktt4S8IFcCoIFYprDIJxVWqmc0e4xKUVWFeyorlSULL4p6Rjc3Sz7x18_z5C2Jq2DhaapuigH4MhUkquFKEkouketb4PwUNlBl-3hd8Zgs3k0ESHZnJoJoeRvz5Uj2UL7o_-lRaBbA-EOOrewJtNP_ourvtP4w9vrnv1</recordid><startdate>2016</startdate><enddate>2016</enddate><creator>Kubin, Minna E.</creator><creator>Hägg, Päivi M.</creator><creator>Kokkonen, Nina</creator><creator>Väyrynen, Juha P.</creator><creator>Haapasaari, Kirsi-Maria</creator><creator>Moilanen, Jyri</creator><creator>Kallioinen, Matti</creator><creator>Hurskainen, Tiina</creator><creator>Tasanen, Kaisa</creator><general>John Libbey Eurotext</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>7X8</scope></search><sort><creationdate>2016</creationdate><title>Glucocorticoid receptors GRα and GRβ are expressed in inflammatory dermatoses</title><author>Kubin, Minna E. ; Hägg, Päivi M. ; Kokkonen, Nina ; Väyrynen, Juha P. ; Haapasaari, Kirsi-Maria ; Moilanen, Jyri ; Kallioinen, Matti ; Hurskainen, Tiina ; Tasanen, Kaisa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c332t-64655d274c274b145e4251258490e5348b9396d1470bc509f7f2688eb3d1487d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adult</topic><topic>Dermatitis - drug therapy</topic><topic>Dermatitis - metabolism</topic><topic>Dermatitis, Atopic - drug therapy</topic><topic>Dermatitis, Atopic - metabolism</topic><topic>Dermatology</topic><topic>Drug Resistance</topic><topic>Eczema - metabolism</topic><topic>Female</topic><topic>Glucocorticoids - therapeutic use</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Investigative Report</topic><topic>Keratinocytes - metabolism</topic><topic>Lichen Planus - metabolism</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Neurodermatitis - metabolism</topic><topic>Neutrophils - metabolism</topic><topic>Prednisolone - therapeutic use</topic><topic>Receptors, Glucocorticoid - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Skin - metabolism</topic><topic>Up-Regulation</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kubin, Minna E.</creatorcontrib><creatorcontrib>Hägg, Päivi M.</creatorcontrib><creatorcontrib>Kokkonen, Nina</creatorcontrib><creatorcontrib>Väyrynen, Juha P.</creatorcontrib><creatorcontrib>Haapasaari, Kirsi-Maria</creatorcontrib><creatorcontrib>Moilanen, Jyri</creatorcontrib><creatorcontrib>Kallioinen, Matti</creatorcontrib><creatorcontrib>Hurskainen, Tiina</creatorcontrib><creatorcontrib>Tasanen, Kaisa</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>EJD. European journal of dermatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kubin, Minna E.</au><au>Hägg, Päivi M.</au><au>Kokkonen, Nina</au><au>Väyrynen, Juha P.</au><au>Haapasaari, Kirsi-Maria</au><au>Moilanen, Jyri</au><au>Kallioinen, Matti</au><au>Hurskainen, Tiina</au><au>Tasanen, Kaisa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glucocorticoid receptors GRα and GRβ are expressed in inflammatory dermatoses</atitle><jtitle>EJD. European journal of dermatology</jtitle><stitle>Eur J Dermatol</stitle><addtitle>Eur J Dermatol</addtitle><date>2016</date><risdate>2016</risdate><volume>26</volume><issue>1</issue><spage>21</spage><epage>27</epage><pages>21-27</pages><issn>1167-1122</issn><eissn>1952-4013</eissn><abstract>Background
Glucocorticoids (GC) are the most commonly used antiinflammatory drugs in dermatology. The actions of GCs are mediated by the glucocorticoid receptor (GR). Alternative splicing of GR mRNA gives rise to different isoforms, GRα and GRβ being the most important. GRβ antagonizes the activity of GRα and its up-regulation has been associated with glucocorticoid insensitivity in several non-cutaneous inflammatory diseases.
Methods
Using immunohistochemical stainings, we analyzed the expression of GRα and GRβ in lesional skin samples of patients with atopic dermatitis, lichen ruber planus, eczema nummulare and lichen simplex chronicus.We also conducted a study of 13 severe atopic patients to investigate the effect of prednisolone treatment on the expression of GR isoforms using quantitative PCR, western blot and immunohistochemical analysis.
Results
GRα and GRβ were expressed in atopic dermatitis, lichen ruber planus, eczema nummulare and lichen simplex chronicus. Our novel finding was that GRα is abundant in keratinocytes and cutaneous neutrophils. Nuclear staining of both GRα and GRβ was strongest in keratinocytes of patients with lichen ruber planus, whereas the least nuclear positivity was detected in keratinocytes of patients with atopic dermatitis. In severe atopic dermatitis GRα and GRβ were expressed in both peripheral blood mononuclear cells and the skin. The expression of GRα and GRβ varied during prednisolone therapy but the changes were not related to treatment response or GC insensitivity.
Conclusion
GRα and GRβ are expressed in inflammatory dermatoses. In severe atopic dermatitis the increased expression of GRβ mRNA is not connected to insensitivity against prednisolone treatment.</abstract><cop>Paris</cop><pub>John Libbey Eurotext</pub><pmid>26711698</pmid><doi>10.1684/ejd.2015.2691</doi><tpages>7</tpages></addata></record> |
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| subjects | Adult Dermatitis - drug therapy Dermatitis - metabolism Dermatitis, Atopic - drug therapy Dermatitis, Atopic - metabolism Dermatology Drug Resistance Eczema - metabolism Female Glucocorticoids - therapeutic use Humans Immunohistochemistry Investigative Report Keratinocytes - metabolism Lichen Planus - metabolism Male Medicine Medicine & Public Health Middle Aged Neurodermatitis - metabolism Neutrophils - metabolism Prednisolone - therapeutic use Receptors, Glucocorticoid - metabolism RNA, Messenger - metabolism Skin - metabolism Up-Regulation Young Adult |
| title | Glucocorticoid receptors GRα and GRβ are expressed in inflammatory dermatoses |
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