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miR-29a Negatively Affects Glucose-Stimulated Insulin Secretion and MIN6 Cell Proliferation via Cdc42β-Catenin Signaling
المؤلفون المشاركون
Duan, Jing
Qian, Xian-Ling
Li, Jun
Xiao, Xing-Hua
Lu, Xiang-Tong
Lv, Lin-Chen
Huang, Qing-Yun
Ding, Wen
Zhang, Hong-Yan
Xiong, Li-Xia
المصدر
International Journal of Endocrinology
العدد
المجلد 2019، العدد 2019 (31 ديسمبر/كانون الأول 2019)، ص ص. 1-13، 13ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2019-08-28
دولة النشر
مصر
عدد الصفحات
13
التخصصات الرئيسية
الملخص EN
Background.
Diabetes is a progressive metabolic disease characterized by hyperglycemia.
Functional impairment of islet β cells can occur to varying degrees.
This impairment can initially be compensated for by proliferation and metabolic changes of β cells.
Cell division control protein 42 (Cdc42) and the microRNA (miRNA) miR-29 have important roles in β-cell proliferation and glucose-stimulated insulin secretion (GSIS), which we further explored using the mouse insulinoma cell line MIN6.
Methods.
Upregulation and downregulation of miR-29a and Cdc42 were accomplished using transient transfection.
miR-29a and Cdc42 expression was detected by real-time PCR and western blotting.
MIN6 proliferation was detected using a cell counting kit assay.
GSIS under high-glucose (20.0 mM) or basal-glucose (5.0 mM) stimulation was detected by enzyme-linked immunosorbent assay.
The miR-29a binding site in the Cdc42 mRNA 3′-untranslated region (UTR) was determined using bioinformatics and luciferase reporter assays.
Results.
miR-29a overexpression inhibited proliferation (P<0.01) and GSIS under high-glucose stimulation (P<0.01).
Cdc42 overexpression promoted proliferation (P<0.05) and GSIS under high-glucose stimulation (P<0.05).
miR-29a overexpression decreased Cdc42 expression (P<0.01), whereas miR-29a downregulation increased Cdc42 expression (P<0.01).
The results showed that the Cdc42 mRNA 3′-UTR is a direct target of miR-29a in vitro.
Additionally, Cdc42 reversed miR-29a-mediated inhibition of proliferation and GSIS (P<0.01).
Furthermore, miR-29a inhibited β-catenin expression (P<0.01), whereas Cdc42 promoted β-catenin expression (P<0.01).
Conclusion.
By negatively regulating Cdc42 and the downstream molecule β-catenin, miR-29a inhibits MIN6 proliferation and insulin secretion.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Duan, Jing& Qian, Xian-Ling& Li, Jun& Xiao, Xing-Hua& Lu, Xiang-Tong& Lv, Lin-Chen…[et al.]. 2019. miR-29a Negatively Affects Glucose-Stimulated Insulin Secretion and MIN6 Cell Proliferation via Cdc42β-Catenin Signaling. International Journal of Endocrinology،Vol. 2019, no. 2019, pp.1-13.
https://search.emarefa.net/detail/BIM-1159590
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Duan, Jing…[et al.]. miR-29a Negatively Affects Glucose-Stimulated Insulin Secretion and MIN6 Cell Proliferation via Cdc42β-Catenin Signaling. International Journal of Endocrinology No. 2019 (2019), pp.1-13.
https://search.emarefa.net/detail/BIM-1159590
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Duan, Jing& Qian, Xian-Ling& Li, Jun& Xiao, Xing-Hua& Lu, Xiang-Tong& Lv, Lin-Chen…[et al.]. miR-29a Negatively Affects Glucose-Stimulated Insulin Secretion and MIN6 Cell Proliferation via Cdc42β-Catenin Signaling. International Journal of Endocrinology. 2019. Vol. 2019, no. 2019, pp.1-13.
https://search.emarefa.net/detail/BIM-1159590
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1159590
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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