scholarly journals Astragalus membranaceus Injection Protects Retinal Ganglion Cells by Regulating the Nerve Growth Factor Signaling Pathway in Experimental Rat Traumatic Optic Neuropathy

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Qiong Wu ◽  
Xinyi Gu ◽  
Xinyan Liu ◽  
Xiaoling Yan ◽  
Liang Liao ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Optic Neuropathy ◽  
Astragalus Membranaceus ◽  
Retinal Ganglion ◽  
Traumatic Optic Neuropathy ◽  
Nerve Growth ◽  
Protein Levels ◽  
Ngf Signaling

Activation of the nerve growth factor (NGF) signaling pathway is a potential method of treatment for retinal ganglion cell (RGC) loss due to traumatic optic neuropathy (TON). The present study aimed to explore the biological effects of injecting Astragalus membranaceus (A. mem) on RGCs in an experimental TON model. Adult male Wistar rats were randomly divided into three groups: sham-operated (SL), model (ML), and A. mem injection (AL). The left eyes of the rats were considered the experimental eyes, and the right eyes served as the controls. AL rats received daily intraperitoneal injections of A. mem (3 mL/kg), whereas ML and SL rats were administered the same volume of normal saline. The TON rat model was induced by optic nerve (ON) transverse quantitative traction. After two-week administration, the number of RGCs was determined using retrograde labeling with Fluoro-Gold. The protein levels of NGF, tyrosine kinase receptor A (TrkA), c-Jun N-terminal protein kinase (JNK), JNK phosphorylation (p-JNK), and nuclear factor kappa-B (NF-κB) were assessed using western blotting. The levels of p75 neurotrophin receptor (p75NTR) and NF-κB DNA binding were examined using real-time PCR and an electrophoretic mobility shift assay. In addition, the concentrations of JNK and p-JNK were assessed using an enzyme-linked immunosorbent assay. Results. The number of RGCs in ML was found to be significantly decreased P < 0.01 relative to both AL and SL, together with the downregulation of NGF P < 0.01 , TrkA P < 0.05 , and NF-κB P < 0.01 ; upregulation of p75NTR mRNA P < 0.01 ; and increased protein levels of JNK P < 0.05 and p-JNK P < 0.05 . Treatment using A. mem injection significantly preserved the density of RGCs in rats with experimental TON and markedly upregulated the proteins of NGF P < 0.01 , TrkA P < 0.05 , and NF-κB P < 0.01 and downregulated the mRNA level of p75NTR P < 0.01 , as well as the proteins of JNK P < 0.05 and p-JNK P < 0.01 . Thus, A. mem injection could reduce RGC death in TON induced by ON transverse quantitative traction by stimulating the NGF signaling pathway.

scholarly journals Acceleration of TAA-Induced Liver Fibrosis by Stress Exposure Is Associated with Upregulation of Nerve Growth Factor and Glycopattern Deviations

2021 ◽  
Vol 22 (10) ◽  
pp. 5055
Author(s):  
Catalina Atorrasagasti ◽  
Flavia Piccioni ◽  
Sophia Borowski ◽  
Irene Tirado-González ◽  
Nancy Freitag ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Liver Fibrosis ◽  
Signaling Pathway ◽  
Liver Damage ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor ◽  
Nerve Growth ◽  
Fibrotic Process ◽  
Ngf Signaling

Liver fibrosis results from many chronic injuries and may often progress to cirrhosis and hepatocellular carcinoma (HCC). In fact, up to 90% of HCC arise in a cirrhotic liver. Conversely, stress is implicated in liver damage, worsening disease outcome. Hence, stress could play a role in disrupting liver homeostasis, a concept that has not been fully explored. Here, in a murine model of TAA-induced liver fibrosis we identified nerve growth factor (NGF) to be a crucial regulator of the stress-induced fibrogenesis signaling pathway as it activates its receptor p75 neurotrophin receptor (p75NTR), increasing liver damage. Additionally, blocking the NGF decreased liver fibrosis whereas treatment with recombinant NGF accelerated the fibrotic process to a similar extent than stress challenge. We further show that the fibrogenesis induced by stress is characterized by specific changes in the hepatoglycocode (increased β1,6GlcNAc-branched complex N-glycans and decreased core 1 O-glycans expression) which are also observed in patients with advanced fibrosis compared to patients with a low level of fibrosis. Our study facilitates an understanding of stress-induced liver injury and identify NGF signaling pathway in early stages of the disease, which contributes to the established fibrogenesis.

scholarly journals The Nerve Growth Factor Signaling and Its Potential as Therapeutic Target for Glaucoma

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Haitao Wang ◽  
Rikang Wang ◽  
Thilini Thrimawithana ◽  
Peter J. Little ◽  
Jiangping Xu ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Ganglion Cells ◽  
Tyrosine Kinase Receptor ◽  
Growth Factor Signaling ◽  
Retinal Ganglion ◽  
Nerve Growth ◽  
Therapeutic Implications ◽  
Beneficial Effects ◽  
Ngf Signaling

Neuroprotective therapies which focus on factors leading to retinal ganglion cells (RGCs) degeneration have been drawing more and more attention. The beneficial effects of nerve growth factor (NGF) on the glaucoma have been recently suggested, but its effects on eye tissue are complex and controversial in various studies. Recent clinical trials of systemically and topically administrated NGF demonstrate that NGF is effective in treating several ocular diseases, including glaucoma. NGF has two receptors named high affinity NGF tyrosine kinase receptor TrkA and low affinity receptor p75NTR. Both receptors exist in cells in retina like RGC (expressing TrkA) and glia cells (expressing p75NTR). NGF functions by binding to TrkA or p75NTR alone or both together. The binding of NGF to TrkA alone in RGC promotes RGC’s survival and proliferation through activation of TrkA and several prosurvival pathways. In contrast, the binding of NGF to p75NTR leads to apoptosis although it also promotes survival in some cases. Binding of NGF to both TrkA and p75NTR at the same time leads to survival in which p75NTR functions as a TrkA helping receptor. This review discusses the current understanding of the NGF signaling in retina and the therapeutic implications in the treatment of glaucoma.

Nerve Growth Factor Modulation of Retinal Ganglion Cell Physiology

2014 ◽  
Vol 229 (9) ◽  
pp. 1130-1133 ◽  
Author(s):  
Gloria Roberti ◽  
Flavio Mantelli ◽  
Ilaria Macchi ◽  
Mina Massaro-Giordano ◽  
Marco Centofanti
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Ganglion Cell ◽  
Retinal Ganglion Cell ◽  
Cell Physiology ◽  
Retinal Ganglion ◽  
Nerve Growth

Nerve growth factor mRNA and protein levels measured in the same tissue from normal and Alzheimer's disease parietal cortex

1996 ◽  
Vol 42 (1) ◽  
pp. 175-178 ◽  
Author(s):  
Margaret Fahnestock ◽  
Samuel A. Scott ◽  
Nathalie Jetté ◽  
Jean A. Weingartner ◽  
Keith A. Crutcher
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Parietal Cortex ◽  
Nerve Growth ◽  
Protein Levels

scholarly journals Nerve growth factor employs multiple pathways to induce primary response genes in PC12 cells.

1992 ◽  
Vol 3 (3) ◽  
pp. 363-371 ◽  
Author(s):  
A Batistatou ◽  
C Volonté ◽  
L A Greene
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Pc12 Cells ◽  
Primary Response ◽  
Purine Analogues ◽  
Signaling Mechanism ◽  
Nerve Growth ◽  
Primary Response Genes ◽  
Run Off ◽  
Ngf Signaling

Nerve growth factor (NGF) leads to neuronal differentiation of PC12 cells and promotes their survival in serum-free medium. Past studies have shown that purine analogues block some of the effects of NGF but not others and thus that they can be used to dissect the mechanistic pathways of its action. In the present work we used 2-aminopurine (2-AP) and 6-thioguanine (6-TG) to examine whether NGF causes activation of primary response genes through a single signaling pathway or via multiple pathways. Northern blot analysis and nuclear run-off transcription assays were used to assess the activation of c-fos, c-jun, TIS1, TIS8, and TIS11 after exposure of PC12 cells to NGF in the presence or absence of 2-AP and 6-TG. Our findings indicate that NGF appears to employ at least three distinct pathways to induce early genes in PC12 cells. This suggests that the NGF signaling mechanism diverges at an early point after interaction of NGF with its receptor.

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