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Articles in PresS, published online ahead of print January 2, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00215.2001
Submitted on July 9, 2001
Accepted on December 28, 2001
1 Department of Surgical Sciences, University of Wisconsin-Madison, School of Veterinary Medicine, Madison, WI, none
2 Department of Surgical Sciences, University of Wisconsin-Madison, School of Veterinary Medicine, Madison, WI, none; Department of Surgery, University of Wisconsin-Madison, School of Medicine, Madison, WI, none
* To whom correspondence should be addressed. E-mail: bjorlind{at}svm.vetmed.wisc.edu.
Nerve growth factor (NGF) is a potent inducer of cell proliferation through autophosphorylation of its high-affinity receptor (trkA). Estrogen also modulates proliferation of cells expressing estrogen receptors (ER). Our previous work showed that urothelial cells express both ER
and ERß, and that trkA, NGF, ER and ERß coexist within bladder mucosa. In this report, we examined interaction between estrogen and NGF relative to cell proliferation using primary cultures of human urothelial cells (HUC). 17ß-estradiol (E2, 50 nM), an ER agonist (16-iodo-17ß-estradiol, 16IE2, 10 nM) and an ERß agonist (genistein, 50 nM ) all stimulated HUC proliferation. These effects were abolished by the estrogen antagonist ICI 182, 780 (100nM). NGF (1-100 ng/ml) also stimulated HUC proliferation, and this effect was abolished by NGF-antiserum (0.1µl/ml) or a trkA antagonist (K252a, 100 nM). HUC proliferation stimulated by E2 was also abolished by NGF-antiserum or K252a. Furthermore, we found E2 stimulated NGF synthesis in HUC, and this effect was inhibited by ICI 182, 780. Immunocytochemical staining and immunoblotting confirmed the expression of ER, ERß, and NGF receptors in HUC. Finally, we observed that treatment of HUC with NGF (50 ng/ml) or E2 (50 nM) stimulated trkA phosphorylation, and this effect was abolished by K252a (100 nM) or NGF-antiserum (0.1µl/ml). Taking together, our data indicate that the effects of ER activation on HUC proliferation at least partly involve modulation by NGF via its high-affinity receptor, trkA.
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