Effect of hydrocortisone on the adenylate cyclase system of the skin—in vitro explant study
Identifieur interne : 001011 ( Istex/Corpus ); précédent : 001010; suivant : 001012Effect of hydrocortisone on the adenylate cyclase system of the skin—in vitro explant study
Auteurs : T. Aoyagi ; K. Umeda ; H. Iizuka ; Y. MiuraSource :
- British Journal of Dermatology [ 0007-0963 ] ; 1981-09.
Abstract
We have previously reported the effect of hydrocortisone (HC) on the adenylate cyclase system of pig epidermis. HC had no effect on the basal level of cyclic AMP but there was an increased adrenalineinduced cyclic AMP accumulation when epidermal slices were incubated for more than 6 h with HC. This incubation did not alter the responsiveness to histamine. We are interested in the effects on epidermal cells of HC, which may act through the adenylate cyclase system. It is well documented that adrenaline, histamine and adenosine stimulate adenylate cyciase and cause an accumulation of cyclic AMP in pig epidermis. An increased cyclic AMP results in the inhibition of mitosis and epidermal outgrowth. Employing the rate of epidermal outgrowth and mitotic index as indicators of cyclic AMP effect, we studied the effect of HC on the adenylate cyclase system. The pretrcatment with HC (100 μM) magnified the inhibitory effect of adrenaline on epidermal outgrowth and mitosis, whereas the inhibitory effeet of histamine or adenosine was not affected by HC. It is suggested that HC induced an increased responsiveness of adenylate cyclase to adrenaline, resulting in a magnified inhibitory effect of adrenaline on epidermal outgrowth and mitosis.
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DOI: 10.1111/j.1365-2133.1981.tb01283.x
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Aoyagi</name><affiliation><mods:affiliation>Department of Dermatology, Hokkaido University School of Medicinej Sapporo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Umeda, K" sort="Umeda, K" uniqKey="Umeda K" first="K." last="Umeda">K. Umeda</name><affiliation><mods:affiliation>Department of Dermatology, Hokkaido University School of Medicinej Sapporo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Iizuka, H" sort="Iizuka, H" uniqKey="Iizuka H" first="H." last="Iizuka">H. Iizuka</name><affiliation><mods:affiliation>Department of Dermatology, Hokkaido University School of Medicinej Sapporo, Japan</mods:affiliation></affiliation></author><author><name sortKey="Miura, Y" sort="Miura, Y" uniqKey="Miura Y" first="Y." last="Miura">Y. 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HC had no effect on the basal level of cyclic AMP but there was an increased adrenalineinduced cyclic AMP accumulation when epidermal slices were incubated for more than 6 h with HC. This incubation did not alter the responsiveness to histamine. We are interested in the effects on epidermal cells of HC, which may act through the adenylate cyclase system. It is well documented that adrenaline, histamine and adenosine stimulate adenylate cyciase and cause an accumulation of cyclic AMP in pig epidermis. An increased cyclic AMP results in the inhibition of mitosis and epidermal outgrowth. Employing the rate of epidermal outgrowth and mitotic index as indicators of cyclic AMP effect, we studied the effect of HC on the adenylate cyclase system. The pretrcatment with HC (100 μM) magnified the inhibitory effect of adrenaline on epidermal outgrowth and mitosis, whereas the inhibitory effeet of histamine or adenosine was not affected by HC. It is suggested that HC induced an increased responsiveness of adenylate cyclase to adrenaline, resulting in a magnified inhibitory effect of adrenaline on epidermal outgrowth and mitosis.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>T. AOYAGI</name><affiliations><json:string>Department of Dermatology, Hokkaido University School of Medicinej Sapporo, Japan</json:string></affiliations></json:item><json:item><name>K. UMEDA</name><affiliations><json:string>Department of Dermatology, Hokkaido University School of Medicinej Sapporo, Japan</json:string></affiliations></json:item><json:item><name>H. IIZUKA</name><affiliations><json:string>Department of Dermatology, Hokkaido University School of Medicinej Sapporo, Japan</json:string></affiliations></json:item><json:item><name>Y. 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HC had no effect on the basal level of cyclic AMP but there was an increased adrenalineinduced cyclic AMP accumulation when epidermal slices were incubated for more than 6 h with HC. This incubation did not alter the responsiveness to histamine. We are interested in the effects on epidermal cells of HC, which may act through the adenylate cyclase system. It is well documented that adrenaline, histamine and adenosine stimulate adenylate cyciase and cause an accumulation of cyclic AMP in pig epidermis. An increased cyclic AMP results in the inhibition of mitosis and epidermal outgrowth. Employing the rate of epidermal outgrowth and mitotic index as indicators of cyclic AMP effect, we studied the effect of HC on the adenylate cyclase system. The pretrcatment with HC (100 μM) magnified the inhibitory effect of adrenaline on epidermal outgrowth and mitosis, whereas the inhibitory effeet of histamine or adenosine was not affected by HC. 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W–7, Sapporo 060, Japan.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K.</namePart><namePart type="family">UMEDA</namePart><affiliation>Department of Dermatology, Hokkaido University School of Medicinej Sapporo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">IIZUKA</namePart><affiliation>Department of Dermatology, Hokkaido University School of Medicinej Sapporo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y.</namePart><namePart type="family">MIURA</namePart><affiliation>Department of Dermatology, Hokkaido University School of Medicinej Sapporo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1981-09</dateIssued><edition>Accepted for publication 3 November 1980</edition><copyrightDate encoding="w3cdtf">1981</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="references">22</extent></physicalDescription><abstract lang="en">We have previously reported the effect of hydrocortisone (HC) on the adenylate cyclase system of pig epidermis. HC had no effect on the basal level of cyclic AMP but there was an increased adrenalineinduced cyclic AMP accumulation when epidermal slices were incubated for more than 6 h with HC. This incubation did not alter the responsiveness to histamine. We are interested in the effects on epidermal cells of HC, which may act through the adenylate cyclase system. It is well documented that adrenaline, histamine and adenosine stimulate adenylate cyciase and cause an accumulation of cyclic AMP in pig epidermis. An increased cyclic AMP results in the inhibition of mitosis and epidermal outgrowth. Employing the rate of epidermal outgrowth and mitotic index as indicators of cyclic AMP effect, we studied the effect of HC on the adenylate cyclase system. The pretrcatment with HC (100 μM) magnified the inhibitory effect of adrenaline on epidermal outgrowth and mitosis, whereas the inhibitory effeet of histamine or adenosine was not affected by HC. It is suggested that HC induced an increased responsiveness of adenylate cyclase to adrenaline, resulting in a magnified inhibitory effect of adrenaline on epidermal outgrowth and mitosis.</abstract><relatedItem type="host"><titleInfo><title>British Journal of Dermatology</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0007-0963</identifier><identifier type="eISSN">1365-2133</identifier><identifier type="DOI">10.1111/(ISSN)1365-2133</identifier><identifier type="PublisherID">BJD</identifier><part><date>1981</date><detail type="volume"><caption>vol.</caption><number>105</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>257</start><end>266</end><total>10</total></extent></part></relatedItem><identifier type="istex">5E33A39802D8E3FF015AC67C67E45DA1D8223631</identifier><identifier type="DOI">10.1111/j.1365-2133.1981.tb01283.x</identifier><identifier type="ArticleID">BJD257</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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