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Articles in PresS, published online ahead of print June 26, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00380.2001
Submitted on December 28, 2001
Accepted on June 19, 2002
1 Department of Pediatrics, University of Wisconsin-Madison, Madison, WI, USA
2 Department of Opthalmology and Visual Sciences, University of Wisconsin-Madison, Madison, WI, USA; Department of Pharmacology, University of Wisconsin-Madison, Madison, WI, USA
* To whom correspondence should be addressed. E-mail: cmsorenson{at}facstaff.wisc.edu.
Cell proliferation, survival and differentiation are carefully orchestrated processes during nephrogenesis which become aberrant during renal cyst formation. Signaling through focal adhesion kinase (FAK) impacts these processes although its role during nephrogenesis requires further delineation. We have previously demonstrated that phosphorylation of FAK and paxillin is not down-regulated in cystic kidneys from bcl-2 -/- mice. Here we examine whether FAK downstream signaling pathways are affected in these cystic kidneys. Cystic kidneys from the bcl-2 -/- mice exhibited sustained phosphorylation of Src and MAPK/Erks (Erk1). However, similar levels of expression were noted for phospho-JNK, PI3-kinase, and its target PKB/Akt in kidneys from P20 bcl-2 +/+ and bcl-2 -/- mice. We also examined expression of the adapter protein Shc, implicated in growth and apoptosis. Expression of p66Shc decreases to low levels in postnatal kidneys while p52/p46 Shc was constitutively expressed during nephrogenesis. Shc expression was similar in normal and cystic kidneys. Therefore, sustained activation of MAPK/Erks through the Src/FAK pathway may contribute to the hyperproliferation observed in cystic kidneys from bcl-2 -/- mice.
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