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cytotoxicity can be achieved through
different signaling pathways in rat mesangial cells
Department of Biochemistry and Biophysics, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104
We reported previously that Ro-318220 blocked expression of
mitogen-activated protein kinase phosphatase-1 (MKP-1) induced by tumor
necrosis factor-
(TNF-) and subsequently caused apopotosis in
mesangial cells (Y.-L. Guo, B. Kang, and J. R. Williamson. J. Biol. Chem. 273: 10362-10366,
1998). These data support our hypothesis that a TNF--inducible
phosphatase may be responsible for preventing sustained activation of
c-Jun NH2-terminal protein kinase
(JNK) and consequent cell death in these cells (Y.-L. Guo, K. Baysal,
B. Kang, L.-J. Yang, and J. R. Williamson. J. Biol. Chem. 273: 4027-4034, 1998). In this study, we
investigated the involvement of protein kinase C (PKC) in regulation of
MKP-1 expression in mesangial cells together with effects on viability.
Although originally characterized as a PKC inhibitor, Ro-318220
inhibited TNF--induced MKP-1 expression through a mechanism other
than blocking the PKC pathway. Furthermore, inhibition of the PKC
pathway neither significantly affected TNF--induced MKP-1 expression nor made cells susceptible to toxic effect of TNF-. Thus PKC activation is not essential for cells to achieve the resistance to
TNF- cytotoxicity displayed by normal mesangial cells. However, activation of PKC by phorbol 12-myristate 13-acetate (PMA) dramatically increased cellular resistance to the apoptotic effect of TNF-. Coincidentally, PMA stimulated MKP-1 expression and suppressed JNK
activation. Therefore, PMA-induced MKP-1 expression may contribute to
the protective effect of PMA. These results provide a mechanistic explanation for previous documentation that PKC activation can rescue
some cells from apopotosis.
apoptosis; mitogen-activated protein kinase; mitogen-activated
protein kinase phosphatase; c-Jun
NH2-terminal protein kinase; tumor
necrosis factor-
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