The stress-activated c-Jun protein kinase (JNK) is stimulated by lipoxygenase pathway product 12-HETE in RIN m5F cells

David Bleich, Songyuan Chen, Yeshao Wen, Jerry L. Nadler

Research output: Contribution to journalArticlepeer-review

28 Scopus citations

Abstract

Cytokine induced pancreatic β-cell destruction seen in Type 1 diabetes and islet graft rejection involves multiple intracellular signaling pathways that directly or indirectly lead to inflammatory damage or programmed cell death. IL-1β has been shown to stimulate the 12-lipoxygenase pathway product 12-HETE, in RIN m5F cells; however, the precise role of 12-LO activation in mediating cytokine effects is not clear. Since the stress-activated protein kinase, JNK, has been linked to cytokine mediated inflammatory actions, we studied the effect of two LO products, 12-HETE and 15-HETE, on JNK activity. We demonstrate that 1 nM 12-HETE stimulates JNK activity, while 1 nM 15-HETE, the 15-lipoxygenase pathway product, does not. These results suggest 12-HETE is a novel upstream signal for IL-1β induced JNK activation in RIN m5F cells.

Original languageEnglish (US)
Pages (from-to)448-451
Number of pages4
JournalBiochemical and Biophysical Research Communications
Volume230
Issue number2
DOIs
StatePublished - Jan 13 1997
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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