scholarly journals Role of nucleolar protein NOM1 in pancreatic islet β cell apoptosis in diabetes

2016 ◽  
Vol 12 (4) ◽  
pp. 2275-2280 ◽  
Author(s):  
Leilei Yu ◽  
Huifeng Wang ◽  
Zhongxiu Guo ◽  
Fenghua Li ◽  
Hong Cui
Keyword(s):  
Pancreatic Islet ◽  
Cell Apoptosis ◽  
Nucleolar Protein ◽  
Β Cell

scholarly journals Deficiency of VCP-Interacting Membrane Selenoprotein (VIMP) Leads to G1 Cell Cycle Arrest and Cell Death in MIN6 Insulinoma Cells

2018 ◽  
Vol 51 (5) ◽  
pp. 2185-2197 ◽  
Author(s):  
Lili Men ◽  
Juan Sun ◽  
Decheng Ren
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Insulin Secretion ◽  
Cell Apoptosis ◽  
Β Cells ◽  
Β Cell ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest ◽  
Insulinoma Cells

Background/Aims: VCP-interacting membrane selenoprotein (VIMP), an ER resident selenoprotein, is highly expressed in β-cells, however, the role of VIMP in β-cells has not been characterized. In this study, we studied the relationship between VIMP deficiency and β-cell survival in MIN6 insulinoma cells. Methods: To determine the role of VIMP in β-cells, lentiviral VIMP shRNAs were used to knock down (KD) expression of VIMP in MIN6 cells. Cell death was quantified by propidium iodide (PI) staining followed by flow cytometric analyses using a FACS Caliber and FlowJo software. Cell apoptosis and proliferation were determined by TUNEL assay and Ki67 staining, respectively. Cell cycle was analyzed after PI staining. Results: The results show that 1) VIMP suppression induces β-cell apoptosis, which is associated with a decrease in Bcl-xL, and the β-cell apoptosis induced by VIMP suppression can be inhibited by overexpression of Bcl-xL; 2) VIMP knockdown (KD) decreases cell proliferation and G1 cell cycle arrest by accumulating p27 and decreasing E2F1; 3) VIMP KD suppresses unfolded protein response (UPR) activation by regulating the IRE1α and PERK pathways; 4) VIMP KD increases insulin secretion. Conclusion: These results suggest that VIMP may function as a novel regulator to modulate β-cell survival, proliferation, cell cycle, UPR and insulin secretion in MIN6 cells.

Effects of streptozotocin on pancreatic islet β-cell apoptosis and glucose metabolism in zebrafish larvae

2020 ◽  
Vol 46 (3) ◽  
pp. 1025-1038
Author(s):  
Xue Wang ◽  
Xue-liang Yang ◽  
Ke-chun Liu ◽  
Wen-long Sheng ◽  
Qing Xia ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Pancreatic Islet ◽  
Cell Apoptosis ◽  
Β Cell ◽  
Zebrafish Larvae

Different role of saturated and unsaturated fatty acids in β-cell apoptosis

2002 ◽  
Vol 299 (5) ◽  
pp. 853-856 ◽  
Author(s):  
Katrin Eitel ◽  
Harald Staiger ◽  
Mathias D Brendel ◽  
Daniel Brandhorst ◽  
Reinhard G Bretzel ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Cell Apoptosis ◽  
Unsaturated Fatty Acids ◽  
Β Cell

scholarly journals Redundant role of the cytochrome c-mediated intrinsic apoptotic pathway in pancreatic β-cells

2011 ◽  
Vol 210 (3) ◽  
pp. 285-292 ◽  
Author(s):  
Diana Choi ◽  
Stephanie A Schroer ◽  
Shun Yan Lu ◽  
Erica P Cai ◽  
Zhenyue Hao ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Apoptosis ◽  
Caspase 8 ◽  
Intrinsic Apoptotic Pathway ◽  
Β Cells ◽  
Β Cell ◽  
Pancreatic Β Cells ◽  
Apoptotic Pathway ◽  
Redundant Role

Cytochrome c is one of the central mediators of the mitochondrial or the intrinsic apoptotic pathway. Mice harboring a ‘knock-in’ mutation of cytochrome c, impairing only its apoptotic function, have permitted studies on the essential role of cytochrome c-mediated apoptosis in various tissue homeostasis. To this end, we examined the role of cytochrome c in pancreatic β-cells under homeostatic conditions and in diabetes models, including those induced by streptozotocin (STZ) and c-Myc. Previous studies have shown that both STZ- and c-Myc-induced β-cell apoptosis is mediated through caspase-3 activation; however, the precise mechanism in these modes of cell death was not characterized. The results of our study show that lack of functional cytochrome c does not affect glucose homeostasis or pancreatic β-cell mass under basal conditions. Moreover, the cytochrome c-mediated intrinsic apoptotic pathway is required for neither STZ- nor c-Myc-induced β-cell death. We also observed that the extrinsic apoptotic pathway mediated through caspase-8 was not essential in c-Myc-induced β-cell destruction. These findings suggest that cytochrome c is not required for STZ-induced β-cell apoptosis and, together with the caspase-8-mediated extrinsic pathway, plays a redundant role in c-Myc-induced β-cell apoptosis.

scholarly journals Protective Role of Complement C3 Against Cytokine-Mediated β-Cell Apoptosis

Endocrinology ◽  
2017 ◽  
Vol 158 (8) ◽  
pp. 2503-2521 ◽  
Author(s):  
Reinaldo S Dos Santos ◽  
Laura Marroqui ◽  
Fabio A Grieco ◽  
Lorella Marselli ◽  
Mara Suleiman ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Protective Role ◽  
Complement C3 ◽  
Β Cell

scholarly journals Effects of first-line diabetes therapy with biguanides, sulphonylurea and thiazolidinediones on the differentiation, proliferation and apoptosis of islet cell populations

2021 ◽  
Author(s):  
D. Sarnobat ◽  
R. C. Moffett ◽  
P. R. Flatt ◽  
A. I. Tarasov
Keyword(s):  
Pancreatic Islet ◽  
Cell Apoptosis ◽  
Islet Cells ◽  
Early Stage ◽  
Proliferative Potential ◽  
Low Doses ◽  
Β Cells ◽  
Β Cell ◽  
Oral Hypoglycaemic Agents ◽  
The Impact

Abstract Aims Metformin, rosiglitazone and sulfonylureas enhance either insulin action or secretion and thus have been used extensively as early stage anti-diabetic medication, independently of the aetiology of the disease. When administered to newly diagnosed diabetes patients, these drugs produce variable results. Here, we examined the effects of the three early stage oral hypoglycaemic agents in mice with diabetes induced by multiple low doses of streptozotocin, focusing specifically on the developmental biology of pancreatic islets. Methods Streptozotocin-treated diabetic mice expressing a fluorescent reporter specifically in pancreatic islet α-cells were administered the biguanide metformin (100 mg/kg), thiazolidinedione rosiglitazone (10 mg/kg), or sulfonylurea tolbutamide (20 mg/kg) for 10 days. We assessed the impact of the treatment on metabolic status of the animals as well as on the morphology, proliferative potential and transdifferentiation of pancreatic islet cells, using immunofluorescence. Results The effect of the therapy on the islet cells varied depending on the drug and included enhanced pancreatic islet β-cell proliferation, in case of metformin and rosiglitazone; de-differentiation of α-cells and β-cell apoptosis with tolbutamide; increased relative number of β-cells and bi-hormonal insulin + glucagon + cells with metformin. These effects were accompanied by normalisation of food and fluid intake with only minor effects on glycaemia at the low doses of the agents employed. Conclusions Our data suggest that metformin and rosiglitazone attenuate the depletion of the β-cell pool in the streptozotocin-induced diabetes, whereas tolbutamide exacerbates the β-cell apoptosis, but is likely to protect β-cells from chronic hyperglycaemia by directly elevating insulin secretion.

scholarly journals Obligatory Role of Early Ca2+ Responses in H2O2-Induced β-Cell Apoptosis

2015 ◽  
Vol 38 (10) ◽  
pp. 1599-1605 ◽  
Author(s):  
Taiji Sato ◽  
Yukiko K. Kaneko ◽  
Toshiaki Sawatani ◽  
Akiko Noguchi ◽  
Tomohisa Ishikawa
Keyword(s):  
Cell Apoptosis ◽  
Β Cell

scholarly journals Autoimmune Diabetes in the NOD Mouse: An Essential Role of Fas-FasL Signaling in β Cell Apoptosis

2003 ◽  
Vol 1005 (1) ◽  
pp. 161-165 ◽  
Author(s):  
DIEGO G. SILVA ◽  
LUIS SOCHA ◽  
BRETT CHARLTON ◽  
WILLIAM COWDEN ◽  
NIKOLAI PETROVSKY
Keyword(s):  
Cell Apoptosis ◽  
Essential Role ◽  
Autoimmune Diabetes ◽  
Nod Mouse ◽  
Β Cell
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