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Am J Physiol Cell Physiol (July 16, 2003). doi:10.1152/ajpcell.00228.2003
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Submitted on June 2, 2003
Accepted on July 15, 2003

PKC{epsilon} is involved in JNK activation that mediates LPS-induced TNF-{alpha}, which induces apoptosis in macrophages

Monica Comalada1, Jordi Xaus1, Annabel F Valledor1, Carlos Lopez-Lopez1, Daniel J Pennington2, and Antonio Celada1*

1 Sciences Park of Barcelona, University of Barcelona, Barcelona 08028, Spain
2 Imperial Cancer Research Fund, London WC2A 3PX, United Kingdom

* To whom correspondence should be addressed. E-mail: acelada{at}ub.edu.

LPS is a powerful stimulator of macrophages and induces apoptosis in these cells. Using primary cultures of bone marrow-derived macrophages, we found that the autocrine production of TNF-{alpha} has a major function in LPS-induced apoptosis. LPS activates PKC and regulates the different Mitogen-activated protein kinases (MAPK). We aimed to determine its involvement either in the secretion of TNF-{alpha} or in the induction of apoptosis. Using specific inhibitors and mice with the gene for PKC{epsilon}disrupted, we found that LPS-induced TNF-{alpha}-dependent apoptosis is mostly mediated by PKC[[epsilon] which is not directly involved in the signaling mechanism of apoptosis but rather in the process of TNF-{alpha} secretion. In our cell model, all three MAPKs were involved in the regulation of TNF-{alpha} secretion, but at different levels. JNK mainly regulates TNF-{alpha} transcription and apoptosis, whereas ERK and p38 contribute towards to the regulation of TNF-{alpha} production, probably through post-transcriptional mechanisms. Only JNK activity is mediated by PKC{epsilon} in response to LPS and so plays a major role in TNF-{alpha} secretion and LPS-induced apoptosis. We demonstrated in macrophages that LPS involving PKC{epsilon} regulates JNK activity and produces TNF-{alpha} which induces apoptosis.




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