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dc.creatorPilipović, Ivan
dc.creatorRadojević, Katarina
dc.creatorPerišić, Milica
dc.creatorKosec, Duško
dc.creatorNacka-Aleksić, Mirjana
dc.creatorĐikić, Jasmina
dc.creatorLeposavić, Gordana
dc.date.accessioned2021-02-18T10:38:56Z
dc.date.available2021-02-18T10:38:56Z
dc.date.issued2012
dc.identifier.issn0958-0670
dc.identifier.urihttp://intor.torlakinstitut.com/handle/123456789/353
dc.description.abstractGlucocorticoids have been shown to modulate the expression of noradrenaline metabolizing enzymes and beta(2)- and alpha(1B)-adrenoceptors in a tissue- and cell- specific manner. In the thymus, apart from extensive sympathetic innervation, a regulatory network has been identified that encompasses catecholamine-containing non-lymphoid and lymphoid cells. We examined a putative role of adrenal- and thymus-derived glucocorticoids in modulation of rat thymic noradrenaline levels and adrenoceptor expression. Seven days postadrenalectomy, the thymic levels of mRNAs encoding tyrosine hydroxylase, dopamine beta-hydroxylase, monoamine oxidase-A and, consequently, noradrenaline were decreased. Catecholamine content was diminished in autofluorescent nerve fibres (judging by the intensity of fluorescence) and thymocytes (considering HPLC measurements of noradrenaline and the frequency of tyrosine hydroxylase-positive cells), while it remained unaltered in non-lymphoid autofluorescent cells. In addition, adrenalectomy diminished the thymocyte expression of beta(2)- and alpha(1B)-adrenoceptors at both mRNA and protein levels. Administration of ketoconazole (an inhibitor of glucocorticoid synthesis/action; 25 mg kg(-1) day(-1), s.c.) to glucocorticoid-deprived rats increased the thymic levels of tyrosine hydroxylase, dopamine beta-hydroxylase and, consequently, noradrenaline. The increased intensity of the autofluorescent cell fluorescence in ketoconazole-treated rats indicated an increase in their catecholamine content, and suggested differential glucocorticoid-mediated regulation of catecholamines in thymic lymphoid and non-lymphoid cells. In addition, ketoconazole increased the thymocyte expression of alpha(1B)-adrenoceptors. Thus, this study indicates that in the thymus, as in some other tissues, glucocorticoids not only act in concert with cateholamines, but they may modulate catecholamine action by tuning thymic catecholamine metabolism and adrenoceptor expression in a cell-specific manner. Additionally, the study indicates a role of thymus-derived glucocorticoids in this modulation.en
dc.publisherWiley-Blackwell, Hoboken
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/175050/RS//
dc.rightsopenAccess
dc.sourceExperimental Physiology
dc.titleCatecholaminergic signalling through thymic nerve fibres, thymocytes and stromal cells is dependent on both circulating and locally synthesized glucocorticoidsen
dc.typearticle
dc.rights.licenseARR
dc.citation.epage1223
dc.citation.issue11
dc.citation.other97(11): 1211-1223
dc.citation.rankM22
dc.citation.spage1211
dc.citation.volume97
dc.identifier.doi10.1113/expphysiol.2012.064899
dc.identifier.fulltexthttp://intor.torlakinstitut.com/bitstream/id/195/350.pdf
dc.identifier.pmid22562811
dc.identifier.rcubconv_298
dc.identifier.scopus2-s2.0-84868213619
dc.identifier.wos000310479700010
dc.type.versionpublishedVersion


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