ArticleDiabetologia2003
Prevention of primary non-function of islet xenografts in autoimmune diabetic NOD mice by anti-inflammatory agents.
Article in Diabetologia, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 44 citations in OpenAlex.
- RNA aptamers specific for transmembrane p24 trafficking protein 6 and Clusterin for the targeted delivery of imaging reagents and RNA therapeutics to human β cells.Nature communications · 2022Article
- Thinking bedside at the bench: the NOD mouse model of T1DM.Nature reviews. Endocrinology · 2015Review
- Pro-inflammatory and pro-oxidant status of pancreatic islet in vitro is controlled by TLR-4 and HO-1 pathways.PloS one · 2014Article
- Article
- Catenarin Prevents Type 1 Diabetes in Nonobese Diabetic Mice via Inhibition of Leukocyte Migration Involving the MEK6/p38 and MEK7/JNK Pathways.Evidence-based complementary and alternative medicine : eCAM · 2012Article
- Eicosanoids, β-cell function, and diabetes.Prostaglandins & other lipid mediators · 2011Review
- Deficiency of Atf3, an adaptive-response gene, protects islets and ameliorates inflammation in a syngeneic mouse transplantation model.Diabetologia · 2010Article
- Interferon regulatory factor-1 is a key transcription factor in murine beta cells under immune attack.Diabetologia · 2009Article
- Altered monocyte cyclo-oxygenase response in non-obese diabetic mice.Clinical and experimental immunology · 2009Article
- Thrombosis and inflammation in intraportal islet transplantation: a review of pathophysiology and emerging therapeutics.Journal of diabetes science and technology · 2008Article
- Resolving the conundrum of islet transplantation by linking metabolic dysregulation, inflammation, and immune regulation.Endocrine reviews · 2008Review
- Challenges and emerging technologies in the immunoisolation of cells and tissues.Advanced drug delivery reviews · 2008Review
- Co-expression of vascular endothelial growth factor and interleukin-1 receptor antagonist improves human islet survival and function.Pharmaceutical research · 2006Article
- Histone deacetylase (HDAC) inhibition as a novel treatment for diabetes mellitus.Molecular medicine (Cambridge, Mass.)Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisHigh levels of inflammation locally in the graft during the initial days after transplantation can cause primary non-function (PNF) of grafted xenogeneic islets in NOD mice. The aim of this study was to explore in a model of spontaneous diabetes, the NOD mouse, the potential of anti-inflammatory agents in the prevention of PNF after xenogeneic islet transplantation.
methodsSpontaneously diabetic NOD mice were transplanted with 300 rat islets. Animals were treated with acetylsalicylic acid (AsA), rofecoxib, TGF-beta or IL-1 receptor antagonist (IL-1ra). Intra-graft expression of inflammation-related molecules was measured by real time PCR 8 h post-transplantation. At the same time point, plasma nitrite levels were measured.
resultsXenogeneic islets transplanted in control spontaneously diabetic mice resulted in PNF in 16 out of 38 mice (42%). Initial graft loss was not altered by administration of rofecoxib (30%) or TGF-beta (25%). AsA reduced the rate of rapid graft loss to 8% ( p<0.05 vs controls) and administration of IL-1ra even totally prevented PNF (0%, p<0.05 vs controls). Furthermore, all therapies prolonged the mean survival time of xenogeneic islet grafts. The inhibition of PNF by AsA was associated with decreased intra-islet levels of inflammation-related molecules (IL-1, TNF-alpha, iNOS, COX-2) and chemokines (MCP-1 and MIP-3alpha). Finally, also a diminished production of systemic nitrite levels was observed in AsA- and IL-1ra-treated islet recipients. CONCLUSIONS/
interpretationThese data show that treatment with AsA or IL-1ra prevents PNF after islet transplantation in spontaneously diabetic NOD mice. Moreover, the involvement of non-specific inflammation is recognized in xenogeneic islet PNF in spontaneously diabetic NOD mice.
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