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Article: α2-Macroglobulin expression in the liver in response to inflammation is mediated by the testis

Titleα2-Macroglobulin expression in the liver in response to inflammation is mediated by the testis
Authors
Issue Date2005
PublisherSociety for Endocrinology. The Journal's web site is located at http://joe.endocrinology-journals.org
Citation
Journal Of Endocrinology, 2005, v. 185 n. 3, p. 497-505 How to Cite?
AbstractEarlier studies have shown that germ cells or germ cell-conditioned media are capable of regulating α2-macroglobulin (α2-MG, a non-specific protease inhibitor) expression by Sertoli cells and hepatocytes cultured in vitro. These results illustrate a possible physiological link between testes and liver regarding α2-MG production. Using a series of surgical procedures including castration, hemicastration, and hepatectomy coupled with Northern blot and immunoblot analyses, we report herein that the surge in α2-MG expression in the liver in response to inflammation is indeed regulated, at least in part, by the testis via testosterone. It was found that hepatectomy induced at least a tenfold increase in the steady-state mRNA and protein production of α2-MG in the liver. However, castration induced a mild but not statistically significant induction of α2-MG in the liver in contrast to sham operation or hemicastration alone, when hemicastration alone could induce liver α2-MG production by almost fourfold. Perhaps most important of all, hepatectomy accompanied by castration significantly reduced the liver α2-MG response to the surgery-induced inflammation compared with hepatectomy alone, illustrating that the removal of the testicles can induce a loss of signal communications between the testis and the liver, rendering a significant loss of the α2-MG response to experimentally induced inflammation in the liver. Interestingly, this lack of response of the liver to surgery-induced inflammation regarding α2-MG production following castration could be restored, at least in part, by using testosterone implants placed subdermally 6 days prior to orchiectomy. Collectively, these results illustrate that a physiological link does indeed exist between the testis and the liver, and that testes per se can influence the liver α2-MG expression in response to inflammation in vivo possibly via testosterone or testosterone-induced biological factor(s). © 2005 Society for Endocrinology.
Persistent Identifierhttp://hdl.handle.net/10722/178891
ISSN
2015 Impact Factor: 4.498
2015 SCImago Journal Rankings: 1.910
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLui, WYen_US
dc.contributor.authorCheng, YHen_US
dc.contributor.authorMruk, DDen_US
dc.contributor.authorCheng, CHen_US
dc.contributor.authorMo, MYen_US
dc.contributor.authorLee, WMen_US
dc.contributor.authorCheng, CYen_US
dc.date.accessioned2012-12-19T09:50:30Z-
dc.date.available2012-12-19T09:50:30Z-
dc.date.issued2005en_US
dc.identifier.citationJournal Of Endocrinology, 2005, v. 185 n. 3, p. 497-505en_US
dc.identifier.issn0022-0795en_US
dc.identifier.urihttp://hdl.handle.net/10722/178891-
dc.description.abstractEarlier studies have shown that germ cells or germ cell-conditioned media are capable of regulating α2-macroglobulin (α2-MG, a non-specific protease inhibitor) expression by Sertoli cells and hepatocytes cultured in vitro. These results illustrate a possible physiological link between testes and liver regarding α2-MG production. Using a series of surgical procedures including castration, hemicastration, and hepatectomy coupled with Northern blot and immunoblot analyses, we report herein that the surge in α2-MG expression in the liver in response to inflammation is indeed regulated, at least in part, by the testis via testosterone. It was found that hepatectomy induced at least a tenfold increase in the steady-state mRNA and protein production of α2-MG in the liver. However, castration induced a mild but not statistically significant induction of α2-MG in the liver in contrast to sham operation or hemicastration alone, when hemicastration alone could induce liver α2-MG production by almost fourfold. Perhaps most important of all, hepatectomy accompanied by castration significantly reduced the liver α2-MG response to the surgery-induced inflammation compared with hepatectomy alone, illustrating that the removal of the testicles can induce a loss of signal communications between the testis and the liver, rendering a significant loss of the α2-MG response to experimentally induced inflammation in the liver. Interestingly, this lack of response of the liver to surgery-induced inflammation regarding α2-MG production following castration could be restored, at least in part, by using testosterone implants placed subdermally 6 days prior to orchiectomy. Collectively, these results illustrate that a physiological link does indeed exist between the testis and the liver, and that testes per se can influence the liver α2-MG expression in response to inflammation in vivo possibly via testosterone or testosterone-induced biological factor(s). © 2005 Society for Endocrinology.en_US
dc.languageengen_US
dc.publisherSociety for Endocrinology. The Journal's web site is located at http://joe.endocrinology-journals.orgen_US
dc.relation.ispartofJournal of Endocrinologyen_US
dc.rightsJournal of Endocrinology. Copyright © Society for Endocrinology.-
dc.subject.meshAnimalsen_US
dc.subject.meshDrug Implantsen_US
dc.subject.meshGene Expression Regulationen_US
dc.subject.meshHepatectomyen_US
dc.subject.meshImmunoblottingen_US
dc.subject.meshInflammationen_US
dc.subject.meshLiver - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshOrchiectomyen_US
dc.subject.meshRna, Messenger - Analysisen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshSurgical Wound Infection - Metabolismen_US
dc.subject.meshTestis - Metabolismen_US
dc.subject.meshTestosterone - Pharmacologyen_US
dc.subject.meshAlpha-Macroglobulins - Analysis - Genetics - Metabolismen_US
dc.titleα2-Macroglobulin expression in the liver in response to inflammation is mediated by the testisen_US
dc.typeArticleen_US
dc.identifier.emailLui, WY: wylui@hku.hken_US
dc.identifier.emailLee, WM: hrszlwm@hku.hken_US
dc.identifier.authorityLui, WY=rp00756en_US
dc.identifier.authorityLee, WM=rp00728en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1677/joe.1.06136en_US
dc.identifier.pmid15930176-
dc.identifier.scopuseid_2-s2.0-21244485432en_US
dc.identifier.hkuros100001-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-21244485432&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume185en_US
dc.identifier.issue3en_US
dc.identifier.spage497en_US
dc.identifier.epage505en_US
dc.identifier.isiWOS:000229857800016-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLui, WY=35220192400en_US
dc.identifier.scopusauthoridCheng, YH=37093704600en_US
dc.identifier.scopusauthoridMruk, DD=6701823934en_US
dc.identifier.scopusauthoridCheng, CH=8630373700en_US
dc.identifier.scopusauthoridMo, MY=7006857340en_US
dc.identifier.scopusauthoridLee, WM=24799156600en_US
dc.identifier.scopusauthoridCheng, CY=7404797787en_US

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