UVC radiation-induced effect on human primary thyroid cell proliferation and HLA-DR expression

dc.contributor.authorKostic I.
dc.contributor.authorToffoletto B.
dc.contributor.authorToller M.
dc.contributor.authorBeltrami C.
dc.contributor.authorAmbesi Impiombato F.
dc.contributor.authorCURCIO, Francesco
dc.date.accessioned2021-04-20T14:58:20Z
dc.date.available2021-04-20T14:58:20Z
dc.date.issued2010
dc.description.abstractThe aim of this study was to examine how UVC irradiation will affect normal human thyroid cell proliferation and HLA-DR expression. Primary human thyroid cells were exposed to UVC (254nm wavelength) irradiation. In some experiments 0.5mM buthionine sulfoximine (BSO) was added. Apoptosis was detected measuring annexin V, proteins involved in apoptotic process (p53, Bax, Bcl-2, caspase 3, and 9) by immunoblot analysis and HLA-DR expression by FACS. UVC induced a cell cycle arrest in G0/G1 phase in the first 24h, accumulation of cells in the S phase 72h after treatment, and an increase of apoptotic cells. BSO pretreatment showed an earlier appearance and a higher percentage of apoptosis. p53, caspase 3 and 9 were increased, while Bax and Bcl-2 were decreased. We also observed a transient significant increase in HLA-DR expression. UVC inhibited cell proliferation and induced apoptosis in normal human primary thyroid cells. An inhibitor of glutathione synthesis induced an earlier appearance and higher percentage of apoptosis suggesting that oxidative stress may play a role. Apoptotis involved components of the intrinsic mitochondrial pathway. A transient increase in HLA-DR expression after UVC irradiation could play a role in inducing AITD. © 2010 Georg Thieme Verlag KG Stuttgart · New York.
dc.identifier.doi10.1055/s-0030-1265215
dc.identifier.issn0018-5043
dc.identifier.scopus2-s2.0-78649316658
dc.identifier.urihttps://scidar.kg.ac.rs/handle/123456789/10138
dc.rightsrestrictedAccess
dc.sourceHormone and Metabolic Research
dc.titleUVC radiation-induced effect on human primary thyroid cell proliferation and HLA-DR expression
dc.typearticle

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