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- Andersson, Annika K.,1974-Uppsala universitet,Institutionen för medicinsk cellbiologi (author)
Role of Inducible Nitric Oxide Synthase and Melatonin in Regulation of β-cell Sensitivity to Cytokines
- BookEnglish2003
Publisher, publication year, extent ...
- Uppsala :Acta Universitatis Upsaliensis,2003
- 58 s.
- electronicrdacarrier
Numbers
- LIBRIS-ID:oai:DiVA.org:uu-3537
- ISBN:9155457045
- https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3537URI
Supplementary language notes
- Language:English
- Summary in:English
Part of subdatabase
- SwePubSwePub
Classification
Series
- Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine,0282-7476 ;1280
Notes
- The mechanisms of β-cell destruction leading to type 1 diabetes are complex and not yet fully understood, but infiltration of the islets of Langerhans by autoreactive immune cells is believed to be important. Activated macrophages and T-cells may then secrete cytokines and free radicals, which could selectively damage the β-cells. Among the cytokines, IL-1β, IFN-γ and TNF-α can induce expression of inducible nitric synthase (iNOS) and cyclooxygenase-2. Subsequent nitric oxide (NO) and prostaglandin E2 (PGE2) formation may impair islet function.In the present study, the ability of melatonin (an antioxidative and immunoregulatory hormone) to protect against β-cell damage induced by streptozotocin (STZ; a diabetogenic and free radical generating substance) or IL-1β exposure was examined. In vitro, melatonin counteracted STZ- but not IL-1β-induced islet suppression, indicating that the protective effect of melatonin is related to interference with free radical generation and DNA damage, rather than NO synthesis. In vivo, non-immune mediated diabetes induced by a single dose of STZ was prevented by melatonin.Furthermore, the effects of proinflammatory cytokines were examined in islets obtained from mice with a targeted deletion of the iNOS gene (iNOS -/- mice) and wild-type controls. The in vitro data obtained show that exposure to IL-1β or (IL-1β + IFN-γ) induce disturbances in the insulin secretory pathway, which were independent of NO or PGE2 production and cell death. Initially after addition, in particular IL-1β seems to be stimulatory for the insulin secretory machinery of iNOS –/- islets, whereas IL-1β acts inhibitory after a prolonged period. Separate experiments suggest that the stimulatory effect of IL-1β involves an increased gene expression of phospholipase D1a/b. In addition, the formation of new insulin molecules appears to be affected, since IL-1β and (IL-1β + IFN-γ) suppressed mRNA expression of both insulin convertase enzymes and insulin itself.
Subject headings and genre
- MEDICIN OCH HÄLSOVETENSKAP Medicinska och farmaceutiska grundvetenskaper Cell- och molekylärbiologi hsv//swe
- MEDICAL AND HEALTH SCIENCES Basic Medicine Cell and Molecular Biology hsv//eng
- Cell biology
- β-cell
- Cyclooxygenase
- Cytokine
- Diabetes
- IFN-γ
- IL-1β
- iNOS
- Insulin
- Melatonin
- Nitric oxide
- Pancreatic islets
- Phospholipase D
- Prostaglandin E2
- Streptozotocin
- Cellbiologi
- Cell biology
- Cellbiologi
Added entries (persons, corporate bodies, meetings, titles ...)
- Sandler, Stellan (thesis advisor)
- Welsh, Nils (thesis advisor)
- Eizirik, Décio L. (thesis advisor)
- Billestrup, Nils,Ph. D.Steno Diabetes Center, Gentofte (opponent)
- Uppsala universitetInstitutionen för medicinsk cellbiologi (creator_code:org_t)
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