Transient induction of Cdk9 is critical is the early stage of myocardial differentiation

Transient induction of Cdk9 is critical is the early stage of myocardial differentiation


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نویسندگان: وحیده طرح ریز , لیلا آب خویی , سهیلا منتظرصاحب

عنوان کنگره / همایش: سومین کنگره بین المللی زیست پزشکی (ICB2019) , Iran (Islamic Republic) , تهران , 2019

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نویسنده ثبت کننده مقاله وحیده طرح ریز
مرحله جاری مقاله تایید نهایی
دانشکده/مرکز مربوطه مرکز تحقیقات پزشکی مولکولی
کد مقاله 70444
عنوان فارسی مقاله Transient induction of Cdk9 is critical is the early stage of myocardial differentiation
عنوان لاتین مقاله Transient induction of Cdk9 is critical is the early stage of myocardial differentiation
نوع ارائه پوسترو سخنرانی
عنوان کنگره / همایش سومین کنگره بین المللی زیست پزشکی (ICB2019)
نوع کنگره / همایش بین المللی
کشور محل برگزاری کنگره/ همایش Iran (Islamic Republic)
شهر محل برگزاری کنگره/ همایش تهران
سال انتشار/ ارائه شمسی 1398
سال انتشار/ارائه میلادی 2019
تاریخ شمسی شروع و خاتمه کنگره/همایش 1398/08/19 الی 1398/09/21
آدرس لینک مقاله/ همایش در شبکه اینترنت
آدرس علمی (Affiliation) نویسنده متقاضی Molecular Medicine Research Center, Biomedicine Institute, Tabriz University of Medical Sciences, Tabriz, Iran

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نویسنده نفر چندم مقاله
وحیده طرح ریزاول
لیلا آب خوییدوم
سهیلا منتظرصاحبسوم

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عنوان متن
کلمات کلیدی, myogenesis, myoblast cells, Cdk9, myocardial differentiation
خلاصه مقالهCdk9 is a member of cyclin-dependent kinases (cdks). It is expressed in human and murine ‎tissues with high levels in terminally differentiated cells. Cdk9 is the catalytic core of the positive ‎transcription elongation factor b (P-TEFb) and the general transcription factor P-TEFb, a master ‎regulator of RNA polymerase (Pol) II, phosphorylates the C-terminal domain (CTD) of Pol II ‎and negative elongation factors to release Pol II from promoter-proximal pausing. Although, ‎Cdk9 does not regulate the cell cycle, however, it promotes RNA synthesis in genetic ‎programmers for cell growth, differentiation and viral pathogenesis. In this research, we ‎investigated the role of Cdk9 in two important myogenesis genes (MyoD and Myogenin) ‎regulation by methylation of their promoters.‎ For overexpression of Cdk9, the PCEP4/CDK9 plasmid was transfected to C2C12 cells. ‎Transfected and control cells were differentiated then, RNAs were extracted from the both of ‎transfected and control cells The Promoters of two important myogenesis genes consist of: MyoD ‎and Myogenin were evaluated in transfected and control C2C12 cells by bisulfite sequencing.‎ Potential regulatory roles of Cdk9 on two important myogenesis genes were investigated. We ‎overexpressed Cdk9 in myoblast C2C12 cells, which resulted in significant induction of with ‎overexpression of Cdk9. We further observed Cdk9-mediated apoptosis in C2C12 cells in ‎transfected cells during differentiation. Cdk9 plays a complex role in myocyte progenitor ‎differentiation and apoptosis by regulating two important myogenic factors MyoD and ‎Myogenesis in both of gene and protein levels. Our results showed that over-expression of Cdk9 ‎directly or indirectly decreases the expression of MyoD and Myogenin level by hypo-methylesion ‎of their promoters and silencing of their expression.‎ In this study, we demonstrate that Cdk9 can regulate myogenic transcription factors. During ‎cardiac differentiation of mouse myoblast C2C12 cells, high Cdk9 expression preceded ‎downregulation of MyoD and Myogenin levels. To investigate potential regulatory roles of Cdk9 ‎on cardiac myogenesis genes, we overexpressed Cdk9 in myoblast C2C12 cells. Our results ‎indicated that, although the expression levels of MyoD and Myogenin as key regulators of ‎myogenesis were increased in early stage of differentiation however, we observed a remarkable ‎decreases in expression levels of MyoD and Myogenin and a hypo-methylation of their promoters. ‎Thus, we assume that over-expression of Cdk9 can to decrease of MyoD and Myogenin ‎expression levels by hypo-methylation of their promoters in its chronic activation.‎

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