| Interleukin-1 receptor antagonist (IL-1Ra) and IL-1Ra producing mesenchymal stem cells as modulators of diabetogenesis. | |
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MedLine Citation:
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PMID: 19845478 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The increase of pro-inflammatory cytokines and oxidative stress leads to beta-cell damage and promotes beta-cells apoptosis, in types I and II of diabetes mellitus. Therefore, blocking of pro-inflammatory cytokines should be an effective way for the treatment of diabetes mellitus. When IL-1 occupies its receptor, various pro-inflammatory events are initiated including the synthesis and releases of chemokines and these chemokines attract neutrophils, macrophages, and lymphocytes that cause tissue inflammation. IL-1Ra is a naturally occurring cytokine and is the inhibitor of IL-1. When IL-1Ra binds to the IL-1 receptor, binding of IL-1 is blocked by IL-1Ra and pro-inflammatory signal from IL-1 receptor is stopped. There are mounting evidences to suggest that anti-inflammatory IL-1Ra reduces the inflammatory effects of IL-1 and preserves cell function in both types of diabetes. Therefore, IL-1Ra maybe a new therapeutic agent for diabetes mellitus types I and II. Mesenchymal stem cells (MSCs) are self-renewable multipotent stromal cells that have immunomodulatory capacity. Recently, well characterized subpopulations of MSCs which express IL-1Ra have been described. IL-1Ra expressed by these MSCs effectively binds to IL-1 receptor and protects tissues from inflammation-induced injuries. It has been previously shown that bone marrow-derived MSC therapy could be considered for the treatment of diabetes mellitus type 1 and complications of diabetes mellitus. This review presents understanding of potential use of IL-1Ra and MSCs as modulators of diabetogenesis. |
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Authors:
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Vladislav Volarevic; Ahmed Al-Qahtani; Nebojsa Arsenijevic; Sladjana Pajovic; Miodrag L Lukic |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Autoimmunity Volume: 43 ISSN: 1607-842X ISO Abbreviation: Autoimmunity Publication Date: 2010 Jun |
Date Detail:
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Created Date: 2010-05-14 Completed Date: 2010-08-24 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8900070 Medline TA: Autoimmunity Country: England |
Other Details:
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Languages: eng Pagination: 255-63 Citation Subset: IM |
Affiliation:
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Faculty of Medicine, Center for Molecular Medicine, University of Kragujevac, Kragujevac, Serbia. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Clinical Trials as Topic Diabetes Mellitus, Type 1 / prevention & control, therapy* Diabetes Mellitus, Type 2 / prevention & control, therapy* Humans Interleukin 1 Receptor Antagonist Protein / metabolism, therapeutic use* Interleukin-1 / antagonists & inhibitors, metabolism Mesenchymal Stem Cells / metabolism* Mice Receptors, Interleukin-1 / metabolism Treatment Outcome |
| Chemical | |
Reg. No./Substance:
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0/Interleukin 1 Receptor Antagonist Protein; 0/Interleukin-1; 0/Receptors, Interleukin-1 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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