Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA232041 | ENA |
REPOSITORIES: ENA
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Project description:Locally released cytokines contribute to beta cell dysfunction and apoptosis in Type 1 diabetes. In vitro exposure of insulin producing INS-1E cells to the cytokines interleukin (IL)-1beta + interferon (IFN) gamma leads to a significant increase in apoptosis. To characterize the genetic networks implicated in beta cell dysfunction and apoptosis and its dependence on nitric oxide (NO) production, we performed a time course analysis using the Affymetrix RG U34A microarry. INS-1E cells were exposed in duplicate to IL-1beta + IFN-gamma for six different time points (1, 2, 4, 8, 12, and 24 h) with or without the inducible NO synthase blocker.
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Project description:Human islets exposed to cytokines IL-1β and IFN-γ
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Project description:In the context of T1 Diabetes, pro-inflammatory cytokines IL-1β and IFN-γ are known to contribute to β-cell apoptosis; The measurement of mRNA expression following β-cell exposure to these cytokines gives a picture of the changes in gene expression characterizing the path to β-cell dysfunction and death. INS1 cell lines were cultured in medium with or without IL-1β and IFN-γ. The samples were collected at various time points for profiling with Affymetrix Rat ST arrays. These experiments were performed on two separate occasions.
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Project description:Cytokines have been shown to play a key role in the destruction of beta cells. In the rat insulinoma cell line (INS-1ab) overexpressing pancreatic duodenum homeobox 1 (Pdx1) increases sensitivity to Interleukin 1b (IL-1b). To elucidate mechanisms of action underlying Pdx1 driven potentiation of beta-cell sensitivity to IL-1β, we performed a microarray analysis of INS-1ab cells with and without Pdx1 overexpression exposed to IL-1β between 2h and 24h.
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