scholarly journals Nerve growth factor and its low-affinity receptor promote Schwann cell migration.

1994 ◽  
Vol 91 (7) ◽  
pp. 2795-2799 ◽  
Author(s):  
E. S. Anton ◽  
G. Weskamp ◽  
L. F. Reichardt ◽  
W. D. Matthew
Keyword(s):  
Cell Migration ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Schwann Cell ◽  
Nerve Growth ◽  
Affinity Receptor ◽  
Schwann Cell Migration

scholarly journals Rapamycin promotes Schwann cell migration and nerve growth factor secretion

2014 ◽  
Vol 9 (6) ◽  
pp. 602 ◽  
Author(s):  
Yixia Yin ◽  
Fang Liu ◽  
Haiwei Zhang ◽  
Kaiming Zhang ◽  
Xinyu Wang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Schwann Cell ◽  
Nerve Growth ◽  
Schwann Cell Migration ◽  
Factor Secretion ◽  
Growth Factor Secretion

Nerve Growth Factor Enhances Nerve Regeneration through Fibronectin Grafts

1996 ◽  
Vol 21 (4) ◽  
pp. 514-522 ◽  
Author(s):  
I. H. WHITWORTH ◽  
R. A. BROWN ◽  
C. J. DORÉ ◽  
P. ANAND ◽  
C. J. GREEN ◽  
...  
Keyword(s):  
Image Analysis ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Schwann Cell ◽  
Nerve Regeneration ◽  
Axonal Regeneration ◽  
Cell Regeneration ◽  
Nerve Growth ◽  
Computerized Image Analysis ◽  
Immunohistochemical Techniques

Soluble fibronectin and nerve growth factor (NGF) promote axonal regeneration when placed in silicone tubes. We investigated the ability of orientated fibronectin mats to bind and release bioactive NGF and the possibility of augmenting axonal regeneration following axotomy by using fibronectin conduits impregnated with NGF. The release of NGF was quantified using a fluorometric ELISA and bioactivity confirmed with a neuronal culture bioassay. Immunohistochemical techniques and computerized image analysis were used to assess the rate and volume of axonal and Schwann cell regeneration. The delivery of NGF to the site of injury produced an increase in the rate ( P≤0.007) and volume ( P≤0.004) of both axonal and Schwann cell regeneration when compared to conduits of plain fibronectin. We conclude that the local delivery of NGF by impregnated fibronectin conduits enhances axonal regeneration.

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
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Nerve Growth ◽  
Affinity Receptor

Estrogen-induced proliferation of urothelial cells is modulated by nerve growth factor

2002 ◽  
Vol 282 (6) ◽  
pp. F1075-F1083 ◽  
Author(s):  
Jian Teng ◽  
Zun-Yi Wang ◽  
Dale E. Bjorling
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Primary Cultures ◽  
Cell Types ◽  
Urothelial Cells ◽  
Nerve Growth ◽  
High Affinity Receptor ◽  
17Β Estradiol ◽  
Affinity Receptor ◽  
Estrogen Antagonist

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.

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