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Topical 11β-Hydroxysteroid Dehydrogenase Type 1 Inhibition Corrects Cutaneous Features of Systemic Glucocorticoid Excess in Female Mice
Abstract Glucocorticoid (GC) excess drives multiple cutaneous adverse effects, including skin thinning and poor wound healing. The ubiquitously expressed enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) activates mouse corticosterone from 11-dehydrocorticosterone (and human cortisol from co...
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| Published in: | Endocrinology (Philadelphia) 2018-01, Vol.159 (1), p.547-556 |
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| container_title | Endocrinology (Philadelphia) |
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| creator | Tiganescu, Ana Hupe, Melanie Uchida, Yoshikazu Mauro, Theadora Elias, Peter M Holleran, Walter M |
| description | Abstract
Glucocorticoid (GC) excess drives multiple cutaneous adverse effects, including skin thinning and poor wound healing. The ubiquitously expressed enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) activates mouse corticosterone from 11-dehydrocorticosterone (and human cortisol from cortisone). We previously demonstrated elevated 11β-HSD1 activity during mouse wound healing, but the interplay between cutaneous 11β-HSD1 and systemic GC excess is unexplored. Here, we examined effects of 11β-HSD1 inhibition by carbenoxolone (CBX) in mice treated with corticosterone (CORT) or vehicle for 6 weeks. Mice were treated bidaily with topical CBX or vehicle (VEH) 7 days before wounding and during wound healing. CORT mice displayed skin thinning and impaired wound healing but also increased epidermal integrity. 11β-HSD1 activity was elevated in unwounded CORT skin and was inhibited by CBX. CORT mice treated with CBX displayed 51%, 59%, and 100% normalization of wound healing, epidermal thickness, and epidermal integrity, respectively. Gene expression studies revealed normalization of interleukin 6, keratinocyte growth factor, collagen 1, collagen 3, matrix metalloproteinase 9, and tissue inhibitor of matrix metalloproteinase 4 by CBX during wound healing. Importantly, proinflammatory cytokine expression and resolution of inflammation were unaffected by 11β-HSD1 inhibition. CBX did not regulate skin function or wound healing in the absence of CORT. Our findings demonstrate that 11β-HSD1 inhibition can limit the cutaneous effects of GC excess, which may improve the safety profile of systemic steroids and the prognosis of chronic wounds.
Topical 11β-hydroxysteroid dehydrogenase type 1 inhibition normalizes steroid-induced skin thinning, epidermal integrity, poor healing, and gene dysregulation despite ongoing systemic steroid exposure. |
| doi_str_mv | 10.1210/en.2017-00607 |
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Glucocorticoid (GC) excess drives multiple cutaneous adverse effects, including skin thinning and poor wound healing. The ubiquitously expressed enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) activates mouse corticosterone from 11-dehydrocorticosterone (and human cortisol from cortisone). We previously demonstrated elevated 11β-HSD1 activity during mouse wound healing, but the interplay between cutaneous 11β-HSD1 and systemic GC excess is unexplored. Here, we examined effects of 11β-HSD1 inhibition by carbenoxolone (CBX) in mice treated with corticosterone (CORT) or vehicle for 6 weeks. Mice were treated bidaily with topical CBX or vehicle (VEH) 7 days before wounding and during wound healing. CORT mice displayed skin thinning and impaired wound healing but also increased epidermal integrity. 11β-HSD1 activity was elevated in unwounded CORT skin and was inhibited by CBX. CORT mice treated with CBX displayed 51%, 59%, and 100% normalization of wound healing, epidermal thickness, and epidermal integrity, respectively. Gene expression studies revealed normalization of interleukin 6, keratinocyte growth factor, collagen 1, collagen 3, matrix metalloproteinase 9, and tissue inhibitor of matrix metalloproteinase 4 by CBX during wound healing. Importantly, proinflammatory cytokine expression and resolution of inflammation were unaffected by 11β-HSD1 inhibition. CBX did not regulate skin function or wound healing in the absence of CORT. Our findings demonstrate that 11β-HSD1 inhibition can limit the cutaneous effects of GC excess, which may improve the safety profile of systemic steroids and the prognosis of chronic wounds.
Topical 11β-hydroxysteroid dehydrogenase type 1 inhibition normalizes steroid-induced skin thinning, epidermal integrity, poor healing, and gene dysregulation despite ongoing systemic steroid exposure.</description><identifier>ISSN: 1945-7170</identifier><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2017-00607</identifier><identifier>PMID: 29087473</identifier><language>eng</language><publisher>Washington, DC: Endocrine Society</publisher><subject>11-beta-Hydroxysteroid Dehydrogenase Type 1 - antagonists & inhibitors ; 11-beta-Hydroxysteroid Dehydrogenase Type 1 - metabolism ; 11β-Hydroxysteroid dehydrogenase ; Administration, Topical ; Animals ; Anti-Inflammatory Agents - poisoning ; Carbenoxolone - administration & dosage ; Carbenoxolone - adverse effects ; Carbenoxolone - therapeutic use ; Collagen ; Corticosterone ; Corticosterone - blood ; Corticosterone - pharmacokinetics ; Corticosterone - poisoning ; Cortisol ; Cortisone ; Cytokines - antagonists & inhibitors ; Cytokines - genetics ; Cytokines - metabolism ; Dehydrogenase ; Dehydrogenases ; Drug Eruptions - drug therapy ; Drug Eruptions - etiology ; Drug Eruptions - metabolism ; Drug Eruptions - pathology ; Endocrinology ; Enzyme Inhibitors - administration & dosage ; Enzyme Inhibitors - adverse effects ; Enzyme Inhibitors - therapeutic use ; Epidermis - drug effects ; Epidermis - immunology ; Epidermis - metabolism ; Epidermis - pathology ; Extracellular Matrix - drug effects ; Extracellular Matrix - immunology ; Extracellular Matrix - metabolism ; Extracellular Matrix - pathology ; Female ; Gene expression ; Gene Expression Profiling ; Gene Expression Regulation - drug effects ; Glucocorticoids ; Glucocorticoids - blood ; Glucocorticoids - pharmacokinetics ; Glucocorticoids - poisoning ; Granulation Tissue - drug effects ; Granulation Tissue - immunology ; Granulation Tissue - metabolism ; Granulation Tissue - pathology ; Growth factors ; Guanylate cyclase ; Hydroxysteroids ; Inflammation ; Integrity ; Interleukin 6 ; Interleukins ; Keratinocyte growth factor ; Matrix metalloproteinase ; Matrix metalloproteinases ; Metalloproteinase ; Mice, Hairless ; Organ Size - drug effects ; Skin ; Skin - drug effects ; Skin - injuries ; Skin - metabolism ; Skin - pathology ; Steroid hormones ; Steroids ; Thinning ; Wound healing ; Wound Healing - drug effects</subject><ispartof>Endocrinology (Philadelphia), 2018-01, Vol.159 (1), p.547-556</ispartof><rights>Copyright © 2018 Endocrine Society 2018</rights><rights>Copyright © 2018 Endocrine Society.</rights><rights>Copyright © 2018 Endocrine Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c378t-22badf245855f674487bede98ec450d9dc904a330665727266f7bf24a6bb960f3</citedby><cites>FETCH-LOGICAL-c378t-22badf245855f674487bede98ec450d9dc904a330665727266f7bf24a6bb960f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,786,790,891,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29087473$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tiganescu, Ana</creatorcontrib><creatorcontrib>Hupe, Melanie</creatorcontrib><creatorcontrib>Uchida, Yoshikazu</creatorcontrib><creatorcontrib>Mauro, Theadora</creatorcontrib><creatorcontrib>Elias, Peter M</creatorcontrib><creatorcontrib>Holleran, Walter M</creatorcontrib><title>Topical 11β-Hydroxysteroid Dehydrogenase Type 1 Inhibition Corrects Cutaneous Features of Systemic Glucocorticoid Excess in Female Mice</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>Abstract
Glucocorticoid (GC) excess drives multiple cutaneous adverse effects, including skin thinning and poor wound healing. The ubiquitously expressed enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) activates mouse corticosterone from 11-dehydrocorticosterone (and human cortisol from cortisone). We previously demonstrated elevated 11β-HSD1 activity during mouse wound healing, but the interplay between cutaneous 11β-HSD1 and systemic GC excess is unexplored. Here, we examined effects of 11β-HSD1 inhibition by carbenoxolone (CBX) in mice treated with corticosterone (CORT) or vehicle for 6 weeks. Mice were treated bidaily with topical CBX or vehicle (VEH) 7 days before wounding and during wound healing. CORT mice displayed skin thinning and impaired wound healing but also increased epidermal integrity. 11β-HSD1 activity was elevated in unwounded CORT skin and was inhibited by CBX. CORT mice treated with CBX displayed 51%, 59%, and 100% normalization of wound healing, epidermal thickness, and epidermal integrity, respectively. Gene expression studies revealed normalization of interleukin 6, keratinocyte growth factor, collagen 1, collagen 3, matrix metalloproteinase 9, and tissue inhibitor of matrix metalloproteinase 4 by CBX during wound healing. Importantly, proinflammatory cytokine expression and resolution of inflammation were unaffected by 11β-HSD1 inhibition. CBX did not regulate skin function or wound healing in the absence of CORT. Our findings demonstrate that 11β-HSD1 inhibition can limit the cutaneous effects of GC excess, which may improve the safety profile of systemic steroids and the prognosis of chronic wounds.
Topical 11β-hydroxysteroid dehydrogenase type 1 inhibition normalizes steroid-induced skin thinning, epidermal integrity, poor healing, and gene dysregulation despite ongoing systemic steroid exposure.</description><subject>11-beta-Hydroxysteroid Dehydrogenase Type 1 - antagonists & inhibitors</subject><subject>11-beta-Hydroxysteroid Dehydrogenase Type 1 - metabolism</subject><subject>11β-Hydroxysteroid dehydrogenase</subject><subject>Administration, Topical</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - poisoning</subject><subject>Carbenoxolone - administration & dosage</subject><subject>Carbenoxolone - adverse effects</subject><subject>Carbenoxolone - therapeutic use</subject><subject>Collagen</subject><subject>Corticosterone</subject><subject>Corticosterone - blood</subject><subject>Corticosterone - pharmacokinetics</subject><subject>Corticosterone - poisoning</subject><subject>Cortisol</subject><subject>Cortisone</subject><subject>Cytokines - antagonists & inhibitors</subject><subject>Cytokines - genetics</subject><subject>Cytokines - metabolism</subject><subject>Dehydrogenase</subject><subject>Dehydrogenases</subject><subject>Drug Eruptions - drug therapy</subject><subject>Drug Eruptions - etiology</subject><subject>Drug Eruptions - metabolism</subject><subject>Drug Eruptions - pathology</subject><subject>Endocrinology</subject><subject>Enzyme Inhibitors - administration & dosage</subject><subject>Enzyme Inhibitors - adverse effects</subject><subject>Enzyme Inhibitors - therapeutic use</subject><subject>Epidermis - drug effects</subject><subject>Epidermis - immunology</subject><subject>Epidermis - metabolism</subject><subject>Epidermis - pathology</subject><subject>Extracellular Matrix - drug effects</subject><subject>Extracellular Matrix - immunology</subject><subject>Extracellular Matrix - metabolism</subject><subject>Extracellular Matrix - pathology</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Glucocorticoids</subject><subject>Glucocorticoids - blood</subject><subject>Glucocorticoids - pharmacokinetics</subject><subject>Glucocorticoids - poisoning</subject><subject>Granulation Tissue - drug effects</subject><subject>Granulation Tissue - immunology</subject><subject>Granulation Tissue - metabolism</subject><subject>Granulation Tissue - pathology</subject><subject>Growth factors</subject><subject>Guanylate cyclase</subject><subject>Hydroxysteroids</subject><subject>Inflammation</subject><subject>Integrity</subject><subject>Interleukin 6</subject><subject>Interleukins</subject><subject>Keratinocyte growth factor</subject><subject>Matrix metalloproteinase</subject><subject>Matrix metalloproteinases</subject><subject>Metalloproteinase</subject><subject>Mice, Hairless</subject><subject>Organ Size - drug effects</subject><subject>Skin</subject><subject>Skin - drug effects</subject><subject>Skin - injuries</subject><subject>Skin - metabolism</subject><subject>Skin - pathology</subject><subject>Steroid hormones</subject><subject>Steroids</subject><subject>Thinning</subject><subject>Wound healing</subject><subject>Wound Healing - drug effects</subject><issn>1945-7170</issn><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp1kstu1DAUhi0EoqVlyRZZYtNNim-xkw0Sml6lIhZM15bjnHRcJXawnarzBjwPD8IzkTClFCRWtnw-fT7HvxF6Q8kxZZS8B3_MCFUFIZKoZ2if1qIsFFXk-ZP9HnqV0i0hVAjBX6I9VpNKCcX30bd1GJ01Pab0x_fiYtvGcL9NGWJwLT6BzXJwA94kwOvtCJjiS79xjcsueLwKMYLNCa-mbDyEKeEzMHmKkHDo8JdFNDiLz_vJBhtidnbRnt5bSAk7P9OD6QF_chYO0YvO9AleP6wH6PrsdL26KK4-n1-uPl4VlqsqF4w1pu2YKKuy7KQSolINtFBXYEVJ2rq1NRGGcyJlqZhiUnaqmXkjm6aWpOMH6MPOO07NAK0Fn6Pp9RjdYOJWB-P03xXvNvom3GkpyppIOguOHgQxfJ0gZT24ZKHvdy-gaT33xqv5shl99w96G6bo5_E044RXopJsERY7ysaQUoTusRlK9JKxBq-XjPWvjGf-7dMJHunfof7pMEzj_1y7_8J_AmrFsM0</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Tiganescu, Ana</creator><creator>Hupe, Melanie</creator><creator>Uchida, Yoshikazu</creator><creator>Mauro, Theadora</creator><creator>Elias, Peter M</creator><creator>Holleran, Walter M</creator><general>Endocrine Society</general><general>Oxford University Press</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>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20180101</creationdate><title>Topical 11β-Hydroxysteroid Dehydrogenase Type 1 Inhibition Corrects Cutaneous Features of Systemic Glucocorticoid Excess in Female Mice</title><author>Tiganescu, Ana ; Hupe, Melanie ; Uchida, Yoshikazu ; Mauro, Theadora ; Elias, Peter M ; Holleran, Walter M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c378t-22badf245855f674487bede98ec450d9dc904a330665727266f7bf24a6bb960f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>11-beta-Hydroxysteroid Dehydrogenase Type 1 - antagonists & inhibitors</topic><topic>11-beta-Hydroxysteroid Dehydrogenase Type 1 - metabolism</topic><topic>11β-Hydroxysteroid dehydrogenase</topic><topic>Administration, Topical</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - poisoning</topic><topic>Carbenoxolone - administration & dosage</topic><topic>Carbenoxolone - adverse effects</topic><topic>Carbenoxolone - therapeutic use</topic><topic>Collagen</topic><topic>Corticosterone</topic><topic>Corticosterone - blood</topic><topic>Corticosterone - pharmacokinetics</topic><topic>Corticosterone - poisoning</topic><topic>Cortisol</topic><topic>Cortisone</topic><topic>Cytokines - antagonists & inhibitors</topic><topic>Cytokines - genetics</topic><topic>Cytokines - metabolism</topic><topic>Dehydrogenase</topic><topic>Dehydrogenases</topic><topic>Drug Eruptions - drug therapy</topic><topic>Drug Eruptions - etiology</topic><topic>Drug Eruptions - metabolism</topic><topic>Drug Eruptions - pathology</topic><topic>Endocrinology</topic><topic>Enzyme Inhibitors - administration & dosage</topic><topic>Enzyme Inhibitors - adverse effects</topic><topic>Enzyme Inhibitors - therapeutic use</topic><topic>Epidermis - drug effects</topic><topic>Epidermis - immunology</topic><topic>Epidermis - metabolism</topic><topic>Epidermis - pathology</topic><topic>Extracellular Matrix - drug effects</topic><topic>Extracellular Matrix - immunology</topic><topic>Extracellular Matrix - metabolism</topic><topic>Extracellular Matrix - pathology</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Glucocorticoids</topic><topic>Glucocorticoids - blood</topic><topic>Glucocorticoids - pharmacokinetics</topic><topic>Glucocorticoids - poisoning</topic><topic>Granulation Tissue - drug effects</topic><topic>Granulation Tissue - immunology</topic><topic>Granulation Tissue - metabolism</topic><topic>Granulation Tissue - pathology</topic><topic>Growth factors</topic><topic>Guanylate cyclase</topic><topic>Hydroxysteroids</topic><topic>Inflammation</topic><topic>Integrity</topic><topic>Interleukin 6</topic><topic>Interleukins</topic><topic>Keratinocyte growth factor</topic><topic>Matrix metalloproteinase</topic><topic>Matrix metalloproteinases</topic><topic>Metalloproteinase</topic><topic>Mice, Hairless</topic><topic>Organ Size - drug effects</topic><topic>Skin</topic><topic>Skin - drug effects</topic><topic>Skin - injuries</topic><topic>Skin - metabolism</topic><topic>Skin - pathology</topic><topic>Steroid hormones</topic><topic>Steroids</topic><topic>Thinning</topic><topic>Wound healing</topic><topic>Wound Healing - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tiganescu, Ana</creatorcontrib><creatorcontrib>Hupe, Melanie</creatorcontrib><creatorcontrib>Uchida, Yoshikazu</creatorcontrib><creatorcontrib>Mauro, Theadora</creatorcontrib><creatorcontrib>Elias, Peter M</creatorcontrib><creatorcontrib>Holleran, Walter M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Endocrinology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tiganescu, Ana</au><au>Hupe, Melanie</au><au>Uchida, Yoshikazu</au><au>Mauro, Theadora</au><au>Elias, Peter M</au><au>Holleran, Walter M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Topical 11β-Hydroxysteroid Dehydrogenase Type 1 Inhibition Corrects Cutaneous Features of Systemic Glucocorticoid Excess in Female Mice</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>159</volume><issue>1</issue><spage>547</spage><epage>556</epage><pages>547-556</pages><issn>1945-7170</issn><issn>0013-7227</issn><eissn>1945-7170</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Abstract
Glucocorticoid (GC) excess drives multiple cutaneous adverse effects, including skin thinning and poor wound healing. The ubiquitously expressed enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) activates mouse corticosterone from 11-dehydrocorticosterone (and human cortisol from cortisone). We previously demonstrated elevated 11β-HSD1 activity during mouse wound healing, but the interplay between cutaneous 11β-HSD1 and systemic GC excess is unexplored. Here, we examined effects of 11β-HSD1 inhibition by carbenoxolone (CBX) in mice treated with corticosterone (CORT) or vehicle for 6 weeks. Mice were treated bidaily with topical CBX or vehicle (VEH) 7 days before wounding and during wound healing. CORT mice displayed skin thinning and impaired wound healing but also increased epidermal integrity. 11β-HSD1 activity was elevated in unwounded CORT skin and was inhibited by CBX. CORT mice treated with CBX displayed 51%, 59%, and 100% normalization of wound healing, epidermal thickness, and epidermal integrity, respectively. Gene expression studies revealed normalization of interleukin 6, keratinocyte growth factor, collagen 1, collagen 3, matrix metalloproteinase 9, and tissue inhibitor of matrix metalloproteinase 4 by CBX during wound healing. Importantly, proinflammatory cytokine expression and resolution of inflammation were unaffected by 11β-HSD1 inhibition. CBX did not regulate skin function or wound healing in the absence of CORT. Our findings demonstrate that 11β-HSD1 inhibition can limit the cutaneous effects of GC excess, which may improve the safety profile of systemic steroids and the prognosis of chronic wounds.
Topical 11β-hydroxysteroid dehydrogenase type 1 inhibition normalizes steroid-induced skin thinning, epidermal integrity, poor healing, and gene dysregulation despite ongoing systemic steroid exposure.</abstract><cop>Washington, DC</cop><pub>Endocrine Society</pub><pmid>29087473</pmid><doi>10.1210/en.2017-00607</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 11-beta-Hydroxysteroid Dehydrogenase Type 1 - antagonists & inhibitors 11-beta-Hydroxysteroid Dehydrogenase Type 1 - metabolism 11β-Hydroxysteroid dehydrogenase Administration, Topical Animals Anti-Inflammatory Agents - poisoning Carbenoxolone - administration & dosage Carbenoxolone - adverse effects Carbenoxolone - therapeutic use Collagen Corticosterone Corticosterone - blood Corticosterone - pharmacokinetics Corticosterone - poisoning Cortisol Cortisone Cytokines - antagonists & inhibitors Cytokines - genetics Cytokines - metabolism Dehydrogenase Dehydrogenases Drug Eruptions - drug therapy Drug Eruptions - etiology Drug Eruptions - metabolism Drug Eruptions - pathology Endocrinology Enzyme Inhibitors - administration & dosage Enzyme Inhibitors - adverse effects Enzyme Inhibitors - therapeutic use Epidermis - drug effects Epidermis - immunology Epidermis - metabolism Epidermis - pathology Extracellular Matrix - drug effects Extracellular Matrix - immunology Extracellular Matrix - metabolism Extracellular Matrix - pathology Female Gene expression Gene Expression Profiling Gene Expression Regulation - drug effects Glucocorticoids Glucocorticoids - blood Glucocorticoids - pharmacokinetics Glucocorticoids - poisoning Granulation Tissue - drug effects Granulation Tissue - immunology Granulation Tissue - metabolism Granulation Tissue - pathology Growth factors Guanylate cyclase Hydroxysteroids Inflammation Integrity Interleukin 6 Interleukins Keratinocyte growth factor Matrix metalloproteinase Matrix metalloproteinases Metalloproteinase Mice, Hairless Organ Size - drug effects Skin Skin - drug effects Skin - injuries Skin - metabolism Skin - pathology Steroid hormones Steroids Thinning Wound healing Wound Healing - drug effects |
| title | Topical 11β-Hydroxysteroid Dehydrogenase Type 1 Inhibition Corrects Cutaneous Features of Systemic Glucocorticoid Excess in Female Mice |
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