Abstract:
:Interleukin-1beta (IL-1beta) has been implicated to play an important role in the autoimmune beta cell lesion of insulin-dependent diabetes mellitus (IDDM) because of its inhibition of insulin secretion, direct islet cytotoxicity and alteration of islet cell antigen expression. We have previously demonstrated that IL-1beta inhibits glutamic acid decarboxylase-65 (GAD-65) and increases heat shock protein-70 (HSP-70) expression in islet cells. IL-1beta stimulates the inducible form of nitric oxide (NO) synthase and the resultant increased NO mediates many of IL-1beta's effects. In this study we investigated the role of the NO pathway in mediating the effects of IL-1beta on GAD-65 and HSP-70 expression and on insulin secretion. Islets isolated from Sprague-Dawley rats were cultured with IL-1beta and aminoguanidine (AG), an inhibitor of inducible NO synthase, individually and in combination for 24 h. Accumulated nitrite production, insulin release and islet expression of GAD-65 and HSP-70 were measured. We found that (1) IL-1beta at 10 U/ml increased nitrite production, inhibited insulin release, increased HSP-70 expression and decreased GAD-65 expression. (2) AG alone at 1 mM/ml had no effect on nitrite production, insulin release, GAD-65 and HSP-70 expression. (3) In combination, AG completely blocked IL-1beta increased nitrite production, reversed IL-1beta inhibited insulin release by approximately 50%, completely reversed IL-1beta increased HSP-70 expression, but did not reverse IL-1beta inhibited GAD-65 expression. Our findings indicate that the effect of IL-1beta on HSP-70 expression is mediated by NO production, whereas a NO-independent pathway is involved in the effect of IL-1beta on GAD-65 expression and insulin secretion.
journal_name
Autoimmunityjournal_title
Autoimmunityauthors
Hao W,Myhre AP,Palmer JPdoi
10.3109/08916939908995378subject
Has Abstractpub_date
1999-01-01 00:00:00pages
93-101issue
2eissn
0891-6934issn
1607-842Xjournal_volume
29pub_type
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