Nerve growth factor stimulates MAPK via the low affinity receptor p75LNTR

FEBS Letters ◽  
1999 ◽  
Vol 463 (3) ◽  
pp. 231-234 ◽  
Author(s):  
Kathrin Susen ◽  
Rolf Heumann ◽  
Andrea Blöchl
2002 ◽  
Vol 282 (6) ◽  
pp. F1075-F1083 ◽  
Author(s):  
Jian Teng ◽  
Zun-Yi Wang ◽  
Dale E. Bjorling

Both nerve growth factor (NGF) and estrogen have been shown to stimulate proliferation of various cell types. Human urothelial cells (HUC) express the α- and β-subtypes of the estrogen receptor (ERαand ERβ) as well as tyrosine kinase A (trkA), the high-affinity receptor for NGF. We investigated interactions between estrogen and NGF relative to cell proliferation using primary cultures of HUC. 17β-estradiol (E2) stimulated NGF synthesis by HUC, and E2 (50 nM), the ERαagonist 16α-iodo-17β-estradiol (10 nM), or the ERβagonist genistein (50 nM) each stimulated HUC proliferation, an effect that was abolished by the estrogen antagonist ICI-182,780 (100 nM). NGF (1–100 ng/ml) stimulated HUC proliferation, and this was abolished by NGF antiserum (0.1 μl/ml) or the trkA antagonist K252a (100 nM). HUC proliferation stimulated by E2 was also abolished by NGF antiserum or K252a. Finally, we observed that treatment of HUC with NGF (50 ng/ml) or E2 (50 nM) stimulated trkA phosphorylation, and this was abolished by K252a (100 nM) or NGF antiserum (0.1 μl/ml). These data indicate that the effects of ER activation on HUC proliferation at least partly involve activation of trkA by NGF.


1997 ◽  
Vol 109 (6) ◽  
pp. 757-764 ◽  
Author(s):  
Carlo Pincelli ◽  
Anne R. Haake ◽  
Luisa Benassi ◽  
Emanuela Grassilli ◽  
Cristina Magnoni ◽  
...  

1999 ◽  
Vol 230 (5) ◽  
pp. 615 ◽  
Author(s):  
Helmut Friess ◽  
Zhao-Wen Zhu ◽  
Fabio F. di Mola ◽  
Christoph Kulli ◽  
Hans U. Graber ◽  
...  

1993 ◽  
Vol 72 (2) ◽  
pp. 237-244 ◽  
Author(s):  
B.C. Figueiredo ◽  
U. Otten ◽  
S. Strauss ◽  
B. Volk ◽  
D. Maysinger

Sign in / Sign up

Export Citation Format

Share Document