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Section II: Beta-Cell Therapeutic Targets Other Than ATP-Sensitive K+ Channels

The Potential Role of SOCS-3 in the Interleukin-1β-Induced Desensitization of Insulin Signaling in Pancreatic Beta-Cells

  1. Brice Emanuelli,
  2. Murielle Glondu,
  3. Chantal Filloux,
  4. Pascal Peraldi and
  5. Emmanuel Van Obberghen
  1. From INSERM U145, Faculty of Medicine, Nice, France
  1. Address correspondence and reprint requests to Emmanuel Van Obberghen, INSERM U145, IFR-50, Faculty of Medicine, 06107 Nice Cedex 2. France. E-mail: vanobbeg{at}unice.fr
Diabetes 2004 Dec; 53(suppl 3): S97-S103. https://doi.org/10.2337/diabetes.53.suppl_3.S97
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  • FIG. 1.
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    FIG. 1.

    IL-1β reduces insulin-induced IR autophosphorylation and IRS tyrosine phosphorylation without affecting IR or IRS expression in RINm5F cells. RINm5F cells were starved overnight then pretreated or not with IL-1β (10 ng/ml) for 2 h. Cells were then stimulated or not with insulin (100 nmol/l) for 5 min and lysed. IRβ subunits and IRS proteins were immunoprecipitated with antibodies recognizing IRβ subunits or both IRS-1 and IRS-2, respectively. An antiphosphotyrosine Western blot was then performed to analyze their tyrosine phosphorylation status. The expression levels of IRβ subunits, IRS-1, or IRS-2 were monitored by anti-IRβ, anti-IRS-1, and anti-IRS-2 Western blot of IR immunoprecipitates and total lysate, respectively. Quantification of IRS tyrosine phosphorylation is expressed as a mean ± SD from six independent experiments. **P < 0.01.

  • FIG. 2.
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    FIG. 2.

    IL-1β inhibits the insulin-induced IRS/p85PI3K complex formation and IRS-associated PI3K activity in RINm5F cells. RINm5F cells were starved overnight then pretreated or not with IL-1β (10 ng/ml) for 2 h. Cells were then stimulated or not with insulin (100 nmol/l) for 5 min and lysed. IRS proteins were immunoprecipitated and then subjected to Western blot or PI3K activity analysis. A: The association of PI3K p85 regulatory subunit with IRS proteins was assessed by an anti-p85PI3K Western blot. Quantification of the presence of PI3K p85 regulatory subunit in IRS immunocomplex is expressed as a mean ± SEM from three independent experiments. **P < 0.01 B: PI3K assay was performed with IRS immunoprecipitates as described in research design and methods.

  • FIG. 3.
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    FIG. 3.

    The inhibitory effect of IL-1β on insulin signaling pathway is not dependent on NO production. RINm5F cells were starved overnight and then submitted to several treatments before insulin stimulation. Cells were pretreated with IL-1β (10 ng/ml) for 2 h in lanes 3–6. In lanes 5 and 6, IL-1β was coincubated with NAME (2 mmol/l). As a control, cells were incubated with NAME alone for 2 h (lanes 7 and 8). Cells were preincubated with SNAP (100 μmol/l) for 1 h (lanes 9 and 10) or 2 h (lanes 11 and 12). Cells were then stimulated or not with insulin (100 nmol/l) for 5 min and lysed. IRS proteins were immunoprecipitated and tyrosine phosphorylation was assessed by an antiphosphotyrosine Western blot.

  • FIG. 4.
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    FIG. 4.

    IL-1β induces SOCS-3 mRNA expression and SOCS-3/IR complex formation in RINm5F cells. RINm5F cells were starved overnight and then stimulated or not with IL-1β (10 ng/ml) for 30 min, 1 h, 2 h, 3 h, or 4 h. A: Total RNA was extracted and analyzed by Northern blot using SOCS-3 as a probe. RNA loading and integrity were verified with an 18S ribosomal probe. Quantification of SOCS-3 mRNA (arbitrary units). B: After 2 h of treatment, total RNA was extracted and analyzed by real-time quantitative PCR using SOCS-3 primers. mRNA expression was normalized using hypoxanthine guanine phosphoribosyl transferase (HPRT) RNA levels. Results are expressed as a mean ± SEM from three independent experiments. C: RINm5F cells were starved overnight then pretreated or not with IL-1β (10 ng/ml) for 2 h. Cells were then stimulated or not with insulin (100 nmol/l) for 5 min and lysed. IRβ subunits were immunoprecipitated with an anti-IRβ antibody. An anti-SOCS-3 Western blot was then performed to analyze the coimmunoprecipitation of SOCS-3 with IRβ subunits. The expression levels of IRβ subunits was monitored by anti-IRβ Western blot of total lysate.

  • FIG. 5.
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    FIG. 5.

    Ectopically expressed SOCS-3 associates with IRβ subunits and decreases insulin-dependent IR autophosphorylation and IRS tyrosine phosphorylation in RINm5F cells. RINm5F cells were infected or not with comparable amounts of GFP-AdV or SOCS-3-AdV. Forty-eight hours after infection, cells were starved overnight then stimulated or not with insulin (100 nmol/l) for 5 min and lysed. A: IRβ subunits were immunoprecipitated with anti-IRβ antibody. Anti-SOCS-3 and antiphosphotyrosine Western blot were then performed. B: IRS proteins were immunoprecipitated with an anti-IRS antibody recognizing both IRS-1 and IRS-2. Tyrosine phosphorylation of these proteins was assessed by an antiphosphotyrosine Western blot. Quantification of IRS tyrosine phosphorylation is expressed as a mean ± SEM from five independent experiments. *P < 0.05. The expression levels of IRβ subunits, IRS-1, and IRS-2 were monitored by anti-IRβ, anti-IRS-1, and anti-IRS-2 Western blot of total lysate, respectively. Ectopically expressed SOCS-3 was revealed after an immunoprecipitation with a rabbit polyclonal anti-SOCS-3 antibody followed by a Western blot with a goat polyclonal anti-SOCS-3 antibody.

  • FIG. 6.
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    FIG. 6.

    SOCS-3 expression inhibits the insulin-induced IRS/p85PI3K complex formation and IRS-associated PI3K activity in RINm5F cells. RINm5F cells were infected or not with comparable amounts of GFP-AdV or SOCS-3-AdV. Forty-eight hours after infection, cells were starved overnight then stimulated or not with insulin (100 nmol/l) for 5 min and lysed. A: IRS proteins were immunoprecipitated with an antibody recognizing both IRS-1 and IRS-2. The association of PI3K p85 regulatory subunit with IRS proteins was assessed by an anti-p85PI3K Western blot. Quantification of PI3K p85 regulatory subunit amount in IRS immunoprecipitates is expressed as a mean ± SEM from five independent experiments. **P < 0.01 B: PI3K activity assay has been performed with IRS immunoprecipitates. Ectopically expressed SOCS-3 was revealed as described in Fig. 5.

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The Potential Role of SOCS-3 in the Interleukin-1β-Induced Desensitization of Insulin Signaling in Pancreatic Beta-Cells
Brice Emanuelli, Murielle Glondu, Chantal Filloux, Pascal Peraldi, Emmanuel Van Obberghen
Diabetes Dec 2004, 53 (suppl 3) S97-S103; DOI: 10.2337/diabetes.53.suppl_3.S97

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The Potential Role of SOCS-3 in the Interleukin-1β-Induced Desensitization of Insulin Signaling in Pancreatic Beta-Cells
Brice Emanuelli, Murielle Glondu, Chantal Filloux, Pascal Peraldi, Emmanuel Van Obberghen
Diabetes Dec 2004, 53 (suppl 3) S97-S103; DOI: 10.2337/diabetes.53.suppl_3.S97
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