Interleukin 1 activates jun N‐terminal kinases JNK1 and JNK2 but not extracellular regulated MAP kinase (ERK) in human glomerular mesangial cells

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Abstract
Interleukin 1 (IL‐1) potently activates human glomerular mesangial cells (HMC). In cytosolic extracts of IL‐1‐stimulated HMC or in anion exchange chromatography fractions we could not find any change in phosphorylation of myelin basic protein (MBP), a good substrate for extracellular regulated kinase (ERK). In contrast, IL‐1 stimulated GST‐jun kinase activity at least 10‐fold. The jun kinase activity could be characterised as JNK1 and JNK2 at the protein and mRNA level. IL‐1, TNF, UV light and osmotic stress, but not PMA, LPS, IL‐3, IL‐4, IL‐6, IL‐8, IL‐10, IL‐13, GM‐CSF, PDGF, bFGF, TGF‐β and interferon‐γ were able to stimulate jun kinase activity in HMC, suggesting that jun kinase is selectively mediating signal transduction of the proinflammatory cytokines IL‐1 and TNF as well as of cellular stress in HMC.