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Cell Journal، جلد ۱۷، شماره Suppl ۱، صفحات ۲۹-۲۹
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عنوان انگلیسی Ps-20: PPAR γ/PGC-1α-FNDC5 Pathway Involvement in Cardiac Differentiation Rate of mESCs
چکیده انگلیسی مقاله Objective: Consistent with necessity of the heart to high energy, the cardiac myocyte differentiation needs a quite high energy which is produced by mitochondria. Peroxisome proliferator-activated receptor (PPAR) γ co-activator 1α (PGC-1α) is a powerful transcriptional regulator of energetic pathways. PGC-1α is attached to PPARγ and accelerates the interaction of this protein with multiple transcription factors. In 2012, Spiegelman and his colleagues introduced Fndc5 as a PGC-1α dependent myokine that was secreted as irisin from the muscle into blood, which caused an increase in energy expenditure. Previous studies showed that transcript levels of Fndc5 were high in heart and skeletal muscles of adult mouse. Our group found that Fndc5 expression is increased during the process of cardiac differentiation of mouse embryonic stem cells (mESCs) similar to PGC1α Materials and Methods: In order to determine the correlation between PGC1α and Fndc5 in cardiac cell differentiation of mESCs, we utilized specific PPARγ agonist and antagonist during precursor cells (CPCs) formation of cardiac differentiation. Results: We assessed that a reduction in PGC1α expression, via treatment with GW9662 during CPCs formation stage, down-regulated FNDC5 transcript levels as well as mitochondrial markers which negatively influenced on the whole process of cardiac differentiation efficiency. On the other hand, increase PGC1α expression during CPCs formation stage via rosiglitazone treatment increases Fndc5 expression level and mitochondrial markers transcription levels which enhanced cardiac differentiation efficiency. Conclusion: We concluded that PPARγ agonist and antagonist induced up and down-regulation of PGC1α and subsequently modulated the process of CPCs formation through an alteration in Fndc5 and mitochondrial markers expression.
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نویسندگان مقاله f قزوینی زادگان | f ghazvini zadegan


k قایدی | k ghaedi


mh نصر اصفهانی | mh nasr esfahani


نشانی اینترنتی http://celljournal.org/journal/article/abstract/76
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