کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8259163 | 1534631 | 2016 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Disrupted dynamics of F-actin and insulin granule fusion in INS-1 832/13 beta-cells exposed to glucotoxicity: partial restoration by glucagon-like peptide 1
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کلمات کلیدی
TIRFMRFPeGFPGSISRRPF-actinNPYVAMP-2SNAREGLP-1VesicleT2DSNAP-25filamentous actin - actin filamentousreserve pool - استخر ذخیرهExocytosis - اگزوسیتوزreadily releasable pool - به راحتی استخر آزادGlucose-stimulated insulin secretion - ترشح انسولین تحریک شده توسط گلوکزType 2 diabetes - دیابت نوع 2Glucotoxicity - سمیت گلوتاتیکTotal internal reflection fluorescence microscopy - میکروسکوپ فلورسانس بازتاب داخلیTarget - هدفVesicle-associated membrane protein 2 - پروتئین غشاء مرتبط با Vesicle 2enhanced green fluorescent protein - پروتئین فلورسنت سبز افزایش یافته استred fluorescent protein - پروتئین فلورسنت قرمزglucagon-like peptide-1 - پپتید 1-گلوکاگون-مانندglucagon-like peptide 1 - پپتید مشابه گلوکاگون 1Control - کنترلHigh-glucose - گلوکز بالاsoluble N-ethylmaleimide-sensitive factor attachment protein receptor - گیرنده پروتئین دلبستگی حساس به پروتئین محلول N-ethylmaleimideNeuropeptide Y - یوروپروتئین Y
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Actin dynamics in pancreatic β-cells is involved in insulin exocytosis but the molecular mechanisms of this dynamics and its role in biphasic insulin secretion in pancreatic β-cells is largely unknown. Moreover, the impact of a glucotoxic environment on the sub-cortical actin network dynamics is poorly studied. In this study, we investigate the behavior of insulin granules and the subcortical actin network dynamics in INS-1 832/13 β-cells submitted to a normal or glucotoxic environment. Our results show that glucose stimulation leads to a reorganization of the subcortical actin network with a rupture of its interactions with t-SNARE proteins (Syntaxin 1A and SNAP-25), promoting insulin secretion in INS-1 832/13 β-cells. Prolonged exposure of INS-1 832/13 β-cells to high-glucose levels (glucotoxicity) leads to the densification of the cortical actin network, which prevents its reorganization under acute glucose, and diminishes the glucose-stimulated insulin secretion, as shown by the decreased number of fusion events. The most interesting in our results is the partial restoration by GLP-1 of the insulin secretion ability from high-glucose treated INS-1 832/13 cells. This improved insulin exocytosis is associated with partial restored actin dynamics and fusion events during the two phases of the secretion, with a preferential involvement of Epac2 signaling in the first phase and a rather involvement of PKA signaling in the second phase of insulin exocytosis. All these data provide some new insights into the mechanism by which current therapeutics may be improving insulin secretion.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1862, Issue 8, August 2016, Pages 1401-1411
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1862, Issue 8, August 2016, Pages 1401-1411
نویسندگان
Aurore Quinault, Blandine Gausseres, Danielle Bailbe, Nella Chebbah, Bernard Portha, Jamileh Movassat, Cecile Tourrel-Cuzin,