Role of miR-200c in Myogenic Differentiation Impairment via p66Shc: Implication in Skeletal Muscle Regeneration of Dystrophic mdx Mice
المؤلفون المشاركون
D’Agostino, M.
Sileno, S.
Torcinaro, Alessio
Marchetti, Lorenza
Beji, Sara
Salis, Chiara
Proietti, Daisy
Imeneo, Giulia
C. Capogrossi, Maurizio
De Santa, Francesca
Magenta, Alessandra
Madaro, Luca
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2018، العدد 2018 (31 ديسمبر/كانون الأول 2018)، ص ص. 1-10، 10ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2018-02-13
دولة النشر
مصر
عدد الصفحات
10
التخصصات الرئيسية
الملخص EN
Duchenne muscular dystrophy (DMD) is a genetic disease associated with mutations of Dystrophin gene that regulate myofiber integrity and muscle degeneration, characterized by oxidative stress increase.
We previously published that reactive oxygen species (ROS) induce miR-200c that is responsible for apoptosis and senescence.
Moreover, we demonstrated that miR-200c increases ROS production and phosphorylates p66Shc in Ser-36.
p66Shc plays an important role in muscle differentiation; we previously showed that p66Shc−/− muscle satellite cells display lower oxidative stress levels and higher proliferation rate and differentiated faster than wild-type (wt) cells.
Moreover, myogenic conversion, induced by MyoD overexpression, is more efficient in p66Shc−/− fibroblasts compared to wt cells.
Herein, we report that miR-200c overexpression in cultured myoblasts impairs skeletal muscle differentiation.
Further, its overexpression in differentiated myotubes decreases differentiation indexes.
Moreover, anti-miR-200c treatment ameliorates myogenic differentiation.
In keeping, we found that miR-200c and p66Shc Ser-36 phosphorylation increase in mdx muscles.
In conclusion, miR-200c inhibits muscle differentiation, whereas its inhibition ameliorates differentiation and its expression levels are increased in mdx mice and in differentiated human myoblasts of DMD.
Therefore, miR-200c might be responsible for muscle wasting and myotube loss, most probably via a p66Shc-dependent mechanism in a pathological disease such as DMD.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
D’Agostino, M.& Torcinaro, Alessio& Madaro, Luca& Marchetti, Lorenza& Sileno, S.& Beji, Sara…[et al.]. 2018. Role of miR-200c in Myogenic Differentiation Impairment via p66Shc: Implication in Skeletal Muscle Regeneration of Dystrophic mdx Mice. Oxidative Medicine and Cellular Longevity،Vol. 2018, no. 2018, pp.1-10.
https://search.emarefa.net/detail/BIM-1211492
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
D’Agostino, M.…[et al.]. Role of miR-200c in Myogenic Differentiation Impairment via p66Shc: Implication in Skeletal Muscle Regeneration of Dystrophic mdx Mice. Oxidative Medicine and Cellular Longevity No. 2018 (2018), pp.1-10.
https://search.emarefa.net/detail/BIM-1211492
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
D’Agostino, M.& Torcinaro, Alessio& Madaro, Luca& Marchetti, Lorenza& Sileno, S.& Beji, Sara…[et al.]. Role of miR-200c in Myogenic Differentiation Impairment via p66Shc: Implication in Skeletal Muscle Regeneration of Dystrophic mdx Mice. Oxidative Medicine and Cellular Longevity. 2018. Vol. 2018, no. 2018, pp.1-10.
https://search.emarefa.net/detail/BIM-1211492
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1211492
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر