scholarly journals Insulin-like growth factor 1 prevents neuronal cell death and paraplegia in the rabbit model of spinal cord ischemia

2001 ◽  
Vol 122 (1) ◽  
pp. 136-143 ◽  
Author(s):  
Yoshihisa Nakao ◽  
Hajime Otani ◽  
Tadashi Yamamura ◽  
Reiji Hattori ◽  
Motohiko Osako ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cell Death ◽  
Growth Factor ◽  
Spinal Cord Ischemia ◽  
Neuronal Cell Death ◽  
Rabbit Model ◽  
Neuronal Cell ◽  
Insulin Like Growth Factor

scholarly journals Fas Receptor and Neuronal Cell Death after Spinal Cord Ischemia

2000 ◽  
Vol 20 (18) ◽  
pp. 6879-6887 ◽  
Author(s):  
Kohji Matsushita ◽  
Yongqin Wu ◽  
Jianhua Qiu ◽  
Loic Lang-Lazdunski ◽  
Lorenz Hirt ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cell Death ◽  
Spinal Cord Ischemia ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Fas Receptor

scholarly journals Hydrogen Sulfide Inhibits Autophagic Neuronal Cell Death by Reducing Oxidative Stress in Spinal Cord Ischemia Reperfusion Injury

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Lei Xie ◽  
Sifei Yu ◽  
Kai Yang ◽  
Changwei Li ◽  
Yu Liang
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Cell Death ◽  
Hydrogen Sulfide ◽  
Motor Function ◽  
Ischemia Reperfusion ◽  
Spinal Cord Ischemia ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Autophagic Cell Death

Autophagy is upregulated in spinal cord ischemia reperfusion (SCIR) injury; however, its expression mechanism is largely unknown; moreover, whether autophagy plays a neuroprotective or neurodegenerative role in SCIR injury remains controversial. To explore these issues, we created an SCIR injury rat model via aortic arch occlusion. Compared with normal controls, autophagic cell death was upregulated in neurons after SCIR injury. We found that autophagy promoted neuronal cell death during SCIR, shown by a significant number of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling- (TUNEL-) positive cells colabeled with the autophagy marker microtubule-associated protein 1 light chain 3, while the autophagy inhibitor 3-methyladenine reduced the number of TUNEL-positive cells and restored neurological and motor function. Additionally, we showed that oxidative stress was the main trigger of autophagic neuronal cell death after SCIR injury and N-acetylcysteine inhibited autophagic cell death and restored neurological and motor function in SCIR injury. Finally, we found that hydrogen sulfide (H2S) inhibited autophagic cell death significantly by reducing oxidative stress in SCIR injury via the AKT-the mammalian target of rapamycin (mTOR) pathway. These findings reveal that oxidative stress induces autophagic cell death and that H2S plays a neuroprotective role by reducing oxidative stress in SCIR.

scholarly journals Linolenic acid prevents neuronal cell death and paraplegia after transient spinal cord ischemia in rats

2003 ◽  
Vol 38 (3) ◽  
pp. 564-575 ◽  
Author(s):  
Loïc Lang-Lazdunski ◽  
Nicolas Blondeau ◽  
Gisèle Jarretou ◽  
Michel Lazdunski ◽  
Catherine Heurteaux
Keyword(s):  
Spinal Cord ◽  
Cell Death ◽  
Linolenic Acid ◽  
Spinal Cord Ischemia ◽  
Neuronal Cell Death ◽  
Neuronal Cell

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.

A-fiber sensory input induces neuronal cell death in the dorsal horn of the adult rat spinal cord

2001 ◽  
Vol 435 (3) ◽  
pp. 276-282 ◽  
Author(s):  
Richard E. Coggeshall ◽  
Helena A. Lekan ◽  
Fletcher A. White ◽  
Clifford J. Woolf
Keyword(s):  
Spinal Cord ◽  
Cell Death ◽  
Dorsal Horn ◽  
Sensory Input ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Rat Spinal Cord ◽  
Adult Rat ◽  
Adult Rat Spinal Cord

Short-term rifampicin pretreatment reduces inflammation and neuronal cell death in a rabbit model of bacterial meningitis*

2009 ◽  
Vol 37 (7) ◽  
pp. 2253-2258 ◽  
Author(s):  
Annette Spreer ◽  
Raimond Lugert ◽  
Valentin Stoltefaut ◽  
Anna Hoecht ◽  
Helmut Eiffert ◽  
...  
Keyword(s):  
Cell Death ◽  
Bacterial Meningitis ◽  
Neuronal Cell Death ◽  
Rabbit Model ◽  
Neuronal Cell ◽  
Short Term

Neuronal Cell Death in the Ischemic Spinal Cord: The Effect of Methylprednisolone

1997 ◽  
Vol 64 (5) ◽  
pp. 1279-1286 ◽  
Author(s):  
Georgios K. Kanellopoulos ◽  
Hiroyuki Kato ◽  
Yingji Wu ◽  
Dimitrios Dougenis ◽  
Mary Mackey ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell
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