کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2580506 1561627 2014 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Tributyltin affects adipogenic cell fate commitment in mesenchymal stem cells by a PPARγ independent mechanism
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم محیط زیست بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
Tributyltin affects adipogenic cell fate commitment in mesenchymal stem cells by a PPARγ independent mechanism
چکیده انگلیسی


• TBT induces adipogenesis by altering cell fate commitment of MSC.
• TBT represses Pref-1 and SOX9, which inhibit adipogenic differentiation of MSC.
• The impact of TBT on early cell fate development does not depend on PPARγ.
• TBT additionally induces PPARγ signaling during final adipogenic differentiation.
• TBT promotes adipogenesis independently and dependently on PPARγ.

The food contaminant tributyltin (TBT) is an endocrine disrupting compound (EDC) promoting adipogenic differentiation in vitro and in vivo. Although prenatal TBT exposure has been shown to induce obesity, the underlying mechanisms and the role of the transcription factor PPARγ are not clarified yet.At different stages of adipogenesis, multipotent murine mesenchymal stem cells (MSC), C3H10T1/2, were exposed to TBT and analyzed for adipogenic differentiation, PPARγ promoter activation and PPARγ1, PPARγ2, Pref-1 and SOX9 expression. Depending on the exposure window, TBT promoted subsequent adipogenesis independently and dependently from PPARγ. In undifferentiated MSC, TBT exposure induced a transcriptional PPARγ-independent repression of Pref-1 and SOX9, which are both suppressors of adipogenic cell fate commitment. During hormonal induction TBT additionally enhanced adipogenic differentiation by PPARγ signaling.The impact of TBT on early cell fate development documents a novel mechanistic insight in the development of adipocytes derived from MSC and its susceptibility to EDC.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Chemico-Biological Interactions - Volume 214, 5 May 2014, Pages 1–9
نویسندگان
, , , ,