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Effects of 17β-Estradiol on Activity, Gene, and Protein Expression of Superoxide Dismutases in Primary Cultured Human Lens Epithelial Cells.

Journal article
Authors Dragana Skiljic
Anne Petersen
Jan-Olof Karlsson
Anders Behndig
Staffan Nilsson
Madeleine Zetterberg
Published in Current eye research
Volume 43
Issue 5
Pages 639-646
ISSN 1460-2202
Publication year 2018
Published at Department of Mathematical Sciences
Institute of Biomedicine
Institute of Neuroscience and Physiology, Department of Clinical Neuroscience
Pages 639-646
Language en
Links dx.doi.org/10.1080/02713683.2018.14...
www.ncbi.nlm.nih.gov/entrez/query.f...
Subject categories Ophthalmology, Cell and Molecular Biology

Abstract

Protective effects of estradiol against H2O2-induced oxidative stress have been demonstrated in lens epithelial cells. The purpose of this study was to investigate the effects of 17β-estradiol (E2) on the different superoxide dismutase (SOD) isoenzymes, SOD-1, SOD-2, and SOD-3, as well as estrogen receptors (ERs), ERα and ERβ, in primary cultured human lens epithelial cells (HLECs).HLECs were exposed to 0.1 µM or 1 µM E2 for 1.5 h and 24 h after which the effects were studied. Protein expression and immunolocalization of SOD-1, SOD-2, ERα, and ERβ were studied with Western blot and immunocytochemistry. Total SOD activity was measured, and gene expression analyses were performed for SOD1, SOD2, and SOD3.Increased SOD activity was seen after 1.5 h exposure to both 0.1 µM and 1 µM E2. There were no significant changes in protein or gene expression of the different SODs. Immunolabeling of SOD-1 was evident in the cytosol and nucleus; whereas, SOD-2 was localized in the mitochondria. Both ERα and ERβ were immunolocalized to the nucleus, and mitochondrial localization of ERβ was evident by colocalization with MitoTracker. Both ERα and ERβ showed altered protein expression levels after exposure to E2.The observed increase in SOD activity after exposure to E2 without accompanying increase in gene or protein expression supports a role for E2 in protection against oxidative stress mediated through non-genomic mechanisms.

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