Nerve growth factor prevents apoptotic cell death in injured central cholinergic neurons

1995 ◽  
Vol 359 (4) ◽  
pp. 573-585 ◽  
Author(s):  
Barbara J. Wilcox ◽  
Michael D. Applegate ◽  
Carlos Portera-Cailliau ◽  
Vassilis E. Koliatsos
Keyword(s):  
Cell Death ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Apoptotic Cell ◽  
Cholinergic Neurons ◽  
Apoptotic Cell Death ◽  
Nerve Growth

scholarly journals v-Crk, an effector of the nerve growth factor signaling pathway, delays apoptotic cell death in neurotrophin-deprived PC12 cells

1996 ◽  
Vol 4 (1) ◽  
pp. 82-93 ◽  
Author(s):  
Robert H Glassman ◽  
Barbara L Hempstead ◽  
Lisa Staiano-Coico ◽  
Melissa G Steiner ◽  
Hidesaburo Hanafusa ◽  
...  
Keyword(s):  
Cell Death ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Pc12 Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Growth Factor Signaling ◽  
Nerve Growth ◽  
Growth Factor Signaling Pathway

Nerve growth factor and ceramides modulate cell death in the early developing inner ear

1998 ◽  
Vol 111 (5) ◽  
pp. 549-556 ◽  
Author(s):  
L.M. Frago ◽  
Y. Leon ◽  
E.J. de la Rosa ◽  
A. Gomez-Munoz ◽  
I. Varela-Nieto
Keyword(s):  
Cell Death ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Inner Ear ◽  
Apoptotic Cell ◽  
Dynamic Balance ◽  
Second Messengers ◽  
Otic Vesicle ◽  
Nerve Growth ◽  
Induced Apoptosis

Regulation of normal development involves a dynamic balance of the mechanisms regulating cell division, differentiation and death. We have investigated the signalling mechanisms involved in regulation of the balance between cell proliferation and apoptotic cell death in the otic vesicle. The sphingomyelin pathway signals apoptosis for nerve growth factor upon binding to p75 receptors. It is initiated by sphingomyelin hydrolysis to generate the second messenger ceramide. In the present study, we show that nerve growth factor stimulates sphingomyelin hydrolysis and the concomitant ceramide release in organotypic cultures of otic vesicles. Both nerve growth factor and ceramide induce apoptotic responses to a different extent. Ceramide-induced apoptosis was suppressed by insulin-like growth factor-I which is a strong promoter of cell growth and morphogenesis for the developing inner ear. In contrast, ceramide-1-phosphate protected the explants from apoptosis induced by serum withdrawal but did not antagonise ceramide-induced cell death. This study suggests that sphingomyelin-derived second messengers might be key modulators of programmed cell death during development.

scholarly journals Pro-Nerve Growth Factor Induces Activation of RhoA Kinase and Neuronal Cell Death

2019 ◽  
Vol 9 (8) ◽  
pp. 204 ◽  
Author(s):  
Marina Sycheva ◽  
Jake Sustarich ◽  
Yuxian Zhang ◽  
Vaithinathan Selvaraju ◽  
Thangiah Geetha ◽  
...  
Keyword(s):  
Cell Death ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Kinase Activity ◽  
Kinase Inhibitor ◽  
Neuronal Cell Death ◽  
Rho Kinase ◽  
Neuronal Cell ◽  
Nerve Growth ◽  
Rhoa Kinase

We have previously shown that the expression of pro-nerve growth factor (proNGF) was significantly increased, nerve growth factor (NGF) level was decreased, and the expression of p75NTR was enhanced in Alzheimer’s disease (AD) hippocampal samples. NGF regulates cell survival and differentiation by binding TrkA and p75NTR receptors. ProNGF is the precursor form of NGF, binds to p75NTR, and induces cell apoptosis. The objective of this study is to determine whether the increased p75NTR expression in AD is due to the accumulation of proNGF and Rho kinase activation. PC12 cells were stimulated with either proNGF or NGF. Pull-down assay was carried out to determine the RhoA kinase activity. We found the expression of p75NTR was enhanced by proNGF compared to NGF. The proNGF stimulation also increased the RhoA kinase activity leading to apoptosis. The expression of active RhoA kinase was found to be increased in human AD hippocampus compared to control. The addition of RhoA kinase inhibitor Y27632 not only blocked the RhoA kinase activity but also reduced the expression of p75NTR receptor and inhibited the activation of JNK and MAPK induced by proNGF. This suggests that overexpression of proNGF in AD enhances p75NTR expression and activation of RhoA, leading to neuronal cell death.

Tunicamycin-Induced Cell Death in the Trigeminal Ganglion is Suppressed by Nerve Growth Factor in the Mouse Embryo

2009 ◽  
Vol 30 (3) ◽  
pp. 461-467
Author(s):  
Hiroyuki Ichikawa ◽  
Bing-Ran Zhao ◽  
Mitsuhiro Kano ◽  
Yoshinaka Shimizu ◽  
Toshihiko Suzuki ◽  
...  
Keyword(s):  
Cell Death ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Trigeminal Ganglion ◽  
Mouse Embryo ◽  
Nerve Growth
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