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

Horm Metab Res. 2010 Nov;42(12):846-53. doi: 10.1055/s-0030-1265215. Epub 2010 Sep 30.

Abstract

The 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 (254 nm wavelength) irradiation. In some experiments 0.5 mM 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 24 h, accumulation of cells in the S phase 72 h 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Caspase 3 / genetics
  • Caspase 3 / metabolism
  • Cell Cycle / drug effects
  • Cell Proliferation / radiation effects*
  • Cells, Cultured
  • Gene Expression / radiation effects*
  • HLA-DR Antigens / genetics*
  • HLA-DR Antigens / metabolism
  • Humans
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Thyroid Gland / cytology*
  • Thyroid Gland / metabolism
  • Thyroid Gland / radiation effects
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism
  • Ultraviolet Rays

Substances

  • HLA-DR Antigens
  • Proto-Oncogene Proteins c-bcl-2
  • Tumor Suppressor Protein p53
  • Caspase 3