ArticleThe Journal of biological chemistry2012
Ciliary neurotrophic factor protects mice against streptozotocin-induced type 1 diabetes through SOCS3: the role of STAT1/STAT3 ratio in β-cell death.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Lycopene ameliorates diabetes-induced pancreatic, hepatic, and renal damage by modulating the JAK/STAT/SOCS signaling pathway in rats.Iranian journal of basic medical sciences · 2025Article
- Article
- Ciliary neurotrophic factor is increased in the plasma of patients with obesity and its levels correlate with diabetes and inflammation indices.Scientific reports · 2022Article
- AAV9-Mediated Cardiac CNTF Overexpression Exacerbated Adverse Cardiac Remodeling in Streptozotocin-Induced Type 1 Diabetic Models.Cardiovascular toxicology · 2022Article
- Biological Effects of Ciliary Neurotrophic Factor on hMADS Adipocytes.Frontiers in endocrinology · 2019Article
- Increased Expression of Circulating microRNA 101-3p in Type 1 Diabetes Patients: New Insights Into miRNA-Regulated Pathophysiological Pathways for Type 1 Diabetes.Frontiers in immunology · 2019Article
- A combination of cytokines EGF and CNTF protects the functional beta cell mass in mice with short-term hyperglycaemia.Diabetologia · 2016Article
- STAT3 modulates β-cell cycling in injured mouse pancreas and protects against DNA damage.Cell death & disease · 2016Article
- Role of ZAC1 in transient neonatal diabetes mellitus and glucose metabolism.World journal of biological chemistry · 2015Review
- Cardiotrophin-1 (CT-1) improves high fat diet-induced cognitive deficits in mice.Neurochemical research · 2015Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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Abstract
Type 1 diabetes is characterized by a loss of islet β-cells. Ciliary neurotrophic factor (CNTF) protects pancreatic islets against cytokine-induced apoptosis. For this reason, we assessed whether CNTF protects mice against streptozotocin-induced diabetes (a model of type 1 diabetes) and the mechanism for this protection. WT and SOCS3 knockdown C57BL6 mice were treated for 5 days with citrate buffer or 0.1 mg/kg CNTF before receiving 80 mg/kg streptozotocin. Glycemia in non-fasted mice was measured weekly from days 0-28 after streptozotocin administration. Diabetes was defined as a blood glucose > 11.2 mmol/liter. Wild-type (WT) and SOCS3 knockdown MIN6 cells were cultured with CNTF, IL1β, or both. CNTF reduced diabetes incidence and islet apoptosis in WT but not in SOCS3kd mice. Likewise, CNTF inhibited apoptosis in WT but not in SOCS3kd MIN6 cells. CNTF increased STAT3 phosphorylation in WT and SOCS3kd mice and MIN6 cells but reduced STAT1 phosphorylation only in WT mice, in contrast to streptozotocin and IL1β. Moreover, CNTF reduced NFκB activation and required down-regulation of inducible NO synthase expression to exert its protective effects. In conclusion, CNTF protects mice against streptozotocin-induced diabetes by increasing pancreatic islet survival, and this protection depends on SOCS3. In addition, SOCS3 expression and β-cell fate are dependent on STAT1/STAT3 ratio.
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