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Volume 272, Number 16, Issue of April 18, 1997 pp. 10877-10881
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

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Interleukin-1 Induction of Mitogen-activated Protein Kinases in Human Mesangial Cells
ROLE OF OXIDATION

(Received for publication, September 16, 1996, and in revised form, December 31, 1996)

From the Department of Medicine, Ohio State University, Columbus, Ohio 43210

Interleukin-1 (IL-1) significantly influences renal cellular function through the induction of several gene products. The molecular mechanisms involved in gene regulation by IL-1 are poorly understood; however, the appearance of novel tyrosine phosphoproteins in IL-1-treated cells suggests that IL-1 may function through tyrosine phosphoprotein intermediates. The mitogen-activated protein (MAP) kinases are tyrosine phosphoproteins that could potentially mediate the effects of IL-1. Protein tyrosine phosphorylation following IL-1 treatment may be dependent on redox changes since the IL-1 receptor is not a protein-tyrosine kinase and oxidation has been shown to induce tyrosine phosphorylation. In this report we demonstrate that conditioning human glomerular mesangial cells with IL-1 results in the tyrosine phosphorylation and activation of two members of the MAP kinase family, extracellular signal-regulated protein kinase 2 (ERK2) and p54 Jun-NH₂-terminal kinase (JNK). This effect of IL-1 is abrogated by pretreating cells with the antioxidants N-acetyl-L-cysteine or dithiothreitol. Furthermore, the effects of IL-1 on ERK and JNK activation are reproduced by treating mesangial cells with membrane-permeable oxidants. IL-1 and oxidants also cause phosphorylation and activation of the upstream ERK regulatory element MAP kinase kinase. Interestingly, IL-1, but not exogenous oxidants, causes phosphorylation of the upstream JNK activator, JNK kinase. These data indicate that IL-1 activates ERK2 through an oxidation-dependent pathway. Exogenous oxidants and IL-1 activate JNK through different upstream mechanisms; however, antioxidant inhibition of JNK activation indicates that endogenous oxidants may play a role in IL-1-induced JNK activation. Thus IL-1 may affect mesangial cell function by activating MAP kinases, which can then regulate gene transcription. Furthermore, reactive oxygen species released during inflammatory glomerular injury may also affect mesangial function through a MAP kinase signal.

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