Source:Molecular and Cellular Endocrinology
Author(s): Romina Oglio, Lisa Thomasz, Leonardo Salvarredi, Guillermo Juvenal, Mario Pisarev
IntroductionTransforming growth factor beta (TGF-β) regulates thyroid function and growth. However, tumoral thyroid cells became resistant to this factor as they undifferentiated. Little is known about the effects of TGF-β isoforms. We compared the role of redox metabolism in the response to TGF-β isoforms between non tumoral and tumoral thyroid cells.Methodology and resultsDifferentiated rat thyroid cells (FRTL-5) and human thyroid follicular carcinoma cells (WRO) were treated with the three isoforms of TGF-β. TGF-β isoforms stopped cell cycle at different steps; G1 for FRTL-5 and G2/M for WRO. The three isoforms decreased cell viability and increased ROS accumulation in both cell lines. These effects were more pronounced in FRTL-5 than in WRO, and the isoform β1 was more potent in ROS production than the other two. TGF-β isoforms decreased total glutathione, catalase expression and it activity in both cell lines. Only in FRTL-5 the lipid peroxidation was demonstrated. Moreover, TGF-β1 decreased glutathione peroxidase and mitochondrial superoxide dismutase mRNA expression and increased mitochondrial ROS in FRTL-5, but no in WRO. Pretreatment with selenium increased glutathione peroxidase activity and decreased ROS production in WRO treated with TGF-β isoforms. Furthermore, selenium partially reversed the effect of TGF-β isoforms on cell viability only in WRO cells. The knockdown of endogenous NOX4 significantly reduced the TGF-β1 effect on cell viability in WRO but no in FRTL-5.ConclusionTGF-β disrupted the redox balance and increased ROS accumulation in both cell lines. FRTL-5 cells showed reduced antioxidant capacity and had a greater sensitivity to TGF-β isoforms, while WRO cells were more resistant. This observation provides new insights into the potential role of TGF-β in the redox regulation of thyroid cells.
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