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Am J Physiol Renal Physiol (June 18, 2002). doi:10.1152/ajprenal.00103.2002
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Articles in PresS, published online ahead of print June 18, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00103.2002
Submitted on March 15, 2002
Accepted on June 10, 2002

Gene Expression Profiling Reveals Role for EGF-Family Ligands in Mesangial Cell Proliferation

Rangnath Mishra1, Patrick Leahy1, and Michael S Simonson1*

1 Department of Medicine, Divisions of Nephrology and CWRU Cancer Center, Case Western Reserve University, University Hospitals of Cleveland, Cleveland, OH, USA

* To whom correspondence should be addressed. E-mail: mss5{at}po.cwru.edu.

Control of mesangial cell growth and matrix accumulation are critical for normal development of the glomerular tuft and for the progression of glomerular injury, but the genes that control mesangial growth are not well understood. We used high-density oligonucleotide microarrays to analyze gene expression in well-differentiated human mesangial cells treated with serum to proliferate. Parallel measurement of >12,000 genes and expressed sequence tags identified 5806 mRNA transcripts in quiescent, unstimulated cells and 609 genes significantly induced or repressed by serum. Functional classification of serum-regulated genes revealed many genes not directly related to cell cycle progression that instead might control renal hemodynamics and glomerular filtration or cause tissue injury, leukocyte exudation, matrix accumulation and fibrosis. Hierarchical cluster analysis defined sets of co-regulated genes with similar functions and identified networks of pro-inflammatory genes with similar expression patterns. Unexpectedly, pathway analysis of the gene expression profile suggested an autocrine role in mesangial proliferation for three growth factors in the epidermal growth factor (EGF) family: heparin-binding EGF-like growth factor, amphiregulin, and epiregulin. A functional role for EGF receptor activation was confirmed by blocking serum-induced proliferation with an EGF receptor-selective kinase inhibitor and with a specific EGF receptor neutralizing antibody. Taken together, these results suggest a role for EGF receptor signaling in control of mesangial cell growth in response to serum.




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