scholarly journals On the Immense Variety and Complexity of Circumstances Conditioning Pancreatic  -Cell Apoptosis in Type 1 Diabetes

Diabetes ◽  
2012 ◽  
Vol 61 (7) ◽  
pp. 1661-1663 ◽  
Author(s):  
D. L. Eizirik ◽  
F. A. Grieco
Keyword(s):  
Type 1 Diabetes ◽  
Cell Apoptosis ◽  
Pancreatic Cell

scholarly journals PTPN2, a Candidate Gene for Type 1 Diabetes, Modulates Pancreatic  -Cell Apoptosis via Regulation of the BH3-Only Protein Bim

Diabetes ◽  
2011 ◽  
Vol 60 (12) ◽  
pp. 3279-3288 ◽  
Author(s):  
I. Santin ◽  
F. Moore ◽  
M. L. Colli ◽  
E. N. Gurzov ◽  
L. Marselli ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Candidate Gene ◽  
Cell Apoptosis ◽  
Pancreatic Cell

scholarly journals PTPN2, a Candidate Gene for Type 1 Diabetes, Modulates Interferon- -Induced Pancreatic  -Cell Apoptosis

Diabetes ◽  
2009 ◽  
Vol 58 (6) ◽  
pp. 1283-1291 ◽  
Author(s):  
F. Moore ◽  
M. L. Colli ◽  
M. Cnop ◽  
M. I. Esteve ◽  
A. K. Cardozo ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Candidate Gene ◽  
Cell Apoptosis ◽  
Pancreatic Cell

scholarly journals Peroxiredoxin 6 Attenuates Alloxan-Induced Type 1 Diabetes Mellitus in Mice and Cytokine-Induced Cytotoxicity in RIN-m5F Beta Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Elena G. Novoselova ◽  
Olga V. Glushkova ◽  
Sergey M. Lunin ◽  
Maxim O. Khrenov ◽  
Svetlana B. Parfenyuk ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Beta Cells ◽  
Cell Apoptosis ◽  
Pancreatic Beta Cells ◽  
Apoptotic Cell ◽  
Main Idea ◽  
Severe Form ◽  
Peroxiredoxin 6 ◽  
Cells Cultured

Type 1 diabetes is associated with the destruction of pancreatic beta cells, which is mediated via an autoimmune mechanism and consequent inflammatory processes. In this article, we describe a beneficial effect of peroxiredoxin 6 (PRDX6) in a type 1 diabetes mouse model. The main idea of this study was based on the well-known data that oxidative stress plays an important role in pathogenesis of diabetes and its associated complications. We hypothesised that PRDX6, which is well known for its various biological functions, including antioxidant activity, may provide an antidiabetic effect. It was shown that PRDX6 prevented hyperglycemia, lowered the mortality rate, restored the plasma cytokine profile, reversed the splenic cell apoptosis, and reduced the β cell destruction in Langerhans islets in mice with a severe form of alloxan-induced diabetes. In addition, PRDX6 protected rat insulinoma RIN-m5F β cells, cultured with TNF-α and IL-1β, against the cytokine-induced cytotoxicity and reduced the apoptotic cell death and production of ROS. Signal transduction studies showed that PRDX6 prevented the activation of NF-κB and c-Jun N-terminal kinase signaling cascades in RIN-m5F β cells cultured with cytokines. In conclusion, there is a prospect for therapeutic application of PRDX6 to delay or even prevent β cell apoptosis in type 1 diabetes.

Rotenone protects against β-cell apoptosis and attenuates type 1 diabetes mellitus

APOPTOSIS ◽  
2019 ◽  
Vol 24 (11-12) ◽  
pp. 879-891 ◽  
Author(s):  
Mengqiu Wu ◽  
Weiyi Chen ◽  
Shengnan Zhang ◽  
Songming Huang ◽  
Aihua Zhang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Cell Apoptosis ◽  
Β Cell

scholarly journals Free fatty acid receptor 2, a candidate target for type 1 diabetes, induces cell apoptosis through ERK signaling

2014 ◽  
Vol 53 (3) ◽  
pp. 367-380 ◽  
Author(s):  
Guojun Shi ◽  
Chen Sun ◽  
Weiqiong Gu ◽  
Minglan Yang ◽  
Xiaofang Zhang ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Glucose Homeostasis ◽  
Cell Apoptosis ◽  
Erk Signaling ◽  
Diabetic Mice ◽  
Acid Receptor ◽  
Free Fatty Acid Receptor

Recent reports have highlighted the roles of free fatty acid receptor 2 (FFAR2) in the regulation of metabolic and inflammatory processes. However, the potential function of FFAR2 in type 1 diabetes (T1D) remains unexplored. Our results indicated that the mRNA level of FFAR2 was upregulated in peripheral blood mononuclear cells of T1D patients. The human FFAR2 promoter regions were cloned, and luciferase reporter assays revealed that NFκB activation induced FFAR2 expression. Furthermore, we showed that FFAR2 activation by overexpression induced cell apoptosis through ERK signaling. Finally, treatment with the FFAR2 agonists acetate or phenylacetamide 1 attenuated the inflammatory response in multiple-low-dose streptozocin-induced diabetic mice, and improved the impaired glucose tolerance. These results indicate that FFAR2 may play a protective role by inducing apoptosis of infiltrated macrophage in the pancreas through its feedback upregulation and activation, thus, in turn, improving glucose homeostasis in diabetic mice. These findings highlight FFAR2 as a potential therapeutic target of T1D, representing a link between immune response and glucose homeostasis.

scholarly journals Deletion of the RNLS Gene using CRISPR/Cas9 as Pancreatic Cell β Protection against Autoimmune and ER Stress for Type 1 Diabetes Mellitus

2021 ◽  
Vol 9 (F) ◽  
pp. 613-619
Author(s):  
Aufa Baraja ◽  
Fadhilla Rachmawati Sunarto ◽  
Arga Setyo Adji ◽  
Fitri Handajani ◽  
Firman Suryadi Rahman
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
B Cells ◽  
Er Stress ◽  
Type 1 Diabetes Mellitus ◽  
Genome Editing ◽  
Immune Recognition ◽  
Pancreatic Cell ◽  
The Unfolded Protein Response

BACKGROUND: Type 1 diabetes mellitus (T1DM) is a chronic disease in children which is usually caused by autoimmunity that damages pancreatic a and b cells which have functions as blood glucose regulators. Some studies stated that Renalase (RNLS) gene deletion will protect these b cells from autoimmune reactions and Endoplasmic Reticulum (ER) stress. RNLS deletion by genome editing Clustered Regular interspersed Short Palindromic Repeats-CRISPR-related (CRISPR/Cas9) is believed to have the potential to be a therapy for T1DM Patients. AIM: This research was conducted to know the potential of RNLS deletion using the CRISPR/Cas9 as an effective therapy and whether it has a permanent effect on T1DM patients. METHODS: The method applied in this research summarized articles by analyzing the titles and abstracts of various predetermined keywords. In this case, the author chose a full-text article published within the past 10 years by prioritizing searches in the last 5 years through PubMed, Google Scholar, Science Direct, Cochrane, American Diabetes Association, and official guidelines from IDAI. RESULTS: RNLS deletion using CRISPR/Cas9 in mice weakened the response of polyclonal -cell-reactive CD8+ T cells and disrupted the immune recognition to cells so that autoimmune killing did occur. In addition, such deletion prevents RNLS ER stress by increasing the threshold, triggering the unfolded protein response so that ER stress is difficult to occur. RNLS mutations in b cells also increase b cell survivability to oxidative stress. CONCLUSION: b cells RNLS deletion by genome editing CRISPR/Cas9 is effective in protecting b cells from autoimmune reactions and RE stress. However, further research is needed to determine the side effects and safety of its use.

Sign in / Sign up

Export Citation Format

Share Document