مورد إلكتروني
Interleukin-1beta-induced alteration in a beta-cell phenotype can reduce cellular sensitivity to conditions that cause necrosis but not to cytokine-induced apoptosis.
| العنوان: | Interleukin-1beta-induced alteration in a beta-cell phenotype can reduce cellular sensitivity to conditions that cause necrosis but not to cytokine-induced apoptosis. |
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| المصدر: | Diabetes (New York, N.Y.), 49 (3 |
| بيانات النشر: | 2000 |
| تفاصيل مُضافة: | Ling, Z Van De Casteele, Christine Eizirik, Decio L. Pipeleers, Daniel |
| نوع الوثيقة: | Electronic Resource |
| مستخلص: | Previous work has shown that interleukin-1beta (IL-1beta) alters protein expression in beta-cells. This alteration is associated with cell death in isolated rat islets but not in isolated rat beta-cells. We examined whether IL-1beta pretreatment of isolated beta-cells influences their sensitivity to toxic agents. After a 24-h culture with IL-1beta (30 U/ml), beta-cells exhibited a lower expression of the beta-cell-specific protein transcription factor pancreatic and duodenal homeobox gene (PDX)-1, glucose transporter GLUT2, and proinsulin convertase PC2, with a marked reduction (60-70%) in glucose-induced insulin production and selective sensitivity to the toxins alloxan (ALX) and streptozotocin (STZ). On the other hand, the cells presented an increased expression of Mn-superoxide dismutase, heat shock protein 70, inducible heme oxygenase, and inducible nitrite oxide synthase. This IL-1beta-induced alteration in beta-cell phenotype resulted in a reduced cellular sensitivity to the beta-cell-specific toxins ALX and STZ; the production of nontoxic conditions of nitric oxide (NO) also rendered the cells less susceptible to radical-induced damage. Exposure to IL-1beta can thus protect beta-cells against conditions that cause necrosis; however, it did not protect against apoptosis induced by the additional presence of interferon-gamma or tumor necrosis factor-alpha. Release of IL-1beta in the endocrine pancreas is thus not necessarily the cause of massive NO-dependent beta-cell destruction. On the contrary, IL-1beta may protect these cells against necrosis, though with a loss of their characteristic phenotype and homeostatic functions. Journal Article Research Support, Non-U.S. Gov't info:eu-repo/semantics/published |
| مصطلحات الفهرس: | Sciences bio-médicales et agricoles, Alloxan -- pharmacology, Animals, Apoptosis -- physiology, Cytokines -- physiology, Dose-Response Relationship, Drug, Interleukin-1 -- pharmacology, Islets of Langerhans -- drug effects, Islets of Langerhans -- pathology, Islets of Langerhans -- physiology, Male, Necrosis, Nitric Oxide Donors -- pharmacology, Osmolar Concentration, Phenotype, Proteins -- metabolism, Rats, Rats, Wistar, Streptozocin -- pharmacology, Triazoles -- pharmacology, info:eu-repo/semantics/article, info:ulb-repo/semantics/articlePeerReview, info:ulb-repo/semantics/openurl/article |
| URL: | |
| الإتاحة: | Open access content. Open access content |
| ملاحظة: | No full-text files English |
| أرقام أخرى: | EQY oai:dipot.ulb.ac.be:2013/52453 uri/info:pmid/10868954 1363712126 |
| المصدر المساهم: | UNIVERSITE LIBRE DE BRUXELLES From OAIster®, provided by the OCLC Cooperative. |
| رقم الأكسشن: | edsoai.on1363712126 |
| قاعدة البيانات: | OAIster |
| الوصف غير متاح. |