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Am J Physiol Renal Physiol (June 11, 2002). doi:10.1152/ajprenal.00181.2002
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Articles in PresS, published online ahead of print June 11, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00181.2002
Submitted on May 9, 2002
Accepted on June 3, 2002

Interaction between MAPK and 12-Lipoxygenase Pathways in Mediating Growth and Matrix Protein Expression in Rat Mesangial Cells

Marpadga A Reddy1, Sharon G Adler2, Young-Sook Kim1, Linda Lanting1, John Rossi3, Shin-Wook Kang2, Jerry L Nadler4, Asha Shahed2, and Rama Natarajan1*

1 Department of Diabetes, Beckman Research Institute of the City of Hope, Duarte, CA, USA
2 Department of Nephrology, Harbor-UCLA Research and Education Institute, Torrance, CA, USA
3 Molecular Biology Department, Beckman Research Institute of the City of Hope, Duarte, CA, USA
4 Department of Endocrinology, University of Virginia Medical School, Charlottsville, VA, USA

* To whom correspondence should be addressed. E-mail: rnatarajan{at}coh.org.

The lipoxygenase (LO) pathway of arachidonate metabolism and mitogen-activated protein kinases (MAPKs) can mediate cellular growth and angiotensin II (AngII) effects in vascular smooth muscle cells. However, their role in renal mesangial cells is not very clear. AngII treatment of rat mesangial cells (RMC) significantly increased 12-LO mRNA expression and formation of the 12-LO product, 12(S)-hydroxyeicosatetraenoic acid (12(S)-HETE) (p<0.03). AngII-induced [3H]-leucine incorporation was blocked by a LO inhibitor, CDC (p<0.02). Furthermore, 12(S)-HETE, directly induced cellular hypertrophy and FN expression (p<0.01) to a similar extent as AngII. Both AngII and 12(S)-HETE led to the activation of p38MAPK and its target transcription factor, CREB. AngII- and 12(S)-HETE-induced CREB activation and [3H]-leucine incorporation were blocked by the p38MAPK inhibitor, SB202190. Furthermore, a specific molecular inhibitor of rat 12-LO mRNA, namely a novel ribozyme, could attenuate Ang II-induced FN mRNA. Thus, p38MAPK-dependent CREB activation may mediate AngII- and LO product-induced FN expression and cellular growth in RMC. Furthermore, AngII effects may be mediated by the LO pathway. These results suggest a novel interaction between LO and p38MAPK activation in MC matrix synthesis associated with renal complications.




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