The Biology of Nerve Growth Factor in Vivo

1988 ◽  
pp. 101-114 ◽  
Author(s):  
Eugene M. Johnson ◽  
Pamela T. Manning ◽  
Christine Wilcox
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Nerve Growth

scholarly journals Gangliosides potentiate in vivo and in vitro effects of nerve growth factor on central cholinergic neurons.

1989 ◽  
Vol 86 (6) ◽  
pp. 2056-2060 ◽  
Author(s):  
A. C. Cuello ◽  
L. Garofalo ◽  
R. L. Kenigsberg ◽  
D. Maysinger
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Cholinergic Neurons ◽  
Nerve Growth ◽  
In Vitro Effects

scholarly journals Cartilage injury regulates nerve growth factor (NGF) in vitro and in vivo and drives painful behaviour in murine OA

2014 ◽  
Vol 22 ◽  
pp. S35
Author(s):  
C. Driscoll ◽  
A. Chanalaris ◽  
C. Knight ◽  
C. Gentry ◽  
S. Bevan ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Cartilage Injury ◽  
Nerve Growth

The in vitro effect of the nerve growth factor on chick embryo spinal ganglia—a light-microscopic evaluation

Development ◽  
1970 ◽  
Vol 24 (2) ◽  
pp. 381-392
Author(s):  
Peddrick Weis
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Chick Embryo ◽  
Culture Period ◽  
Spinal Ganglia ◽  
Nerve Growth ◽  
Microscopic Evaluation ◽  
Vitro Effect

The effect of the nerve growth factor (NGF) on chick embryo spinal ganglia was studied in the hanging-drop bioassay system by comparison with parallel development in vivo. The well-differentiated ventrolateral neuroblasts, which in vivo increase 1·33 times in size during the culture period, did not increase in size at all in vitro. Only 65–72% survived to the end of the culture period regardless of the NGF concentration. The less-differentiated mediodorsal (M-D) neuroblasts, which in vivo increase 1·31 times in size during the culture period, were found to increase equally in vitro if sufficient NGF was present. Such a quantity was greater than that which evoked maximum outgrowth of neurites. Survival of M-D neuroblasts was also related to NGF concentration but did not equal the in vivo condition even at the highest concentration. The hyperchromatic type of degeneration prevented by high NGF concentrations is that which results in vivo from insufficient peripheral field. From this and other reports it would appear that the response to NGF seen in vitro is due only to the M-D neuroblasts, and that all biochemical and cytological observations which have been reported would therefore represent conditions within those cells only.

scholarly journals Multiple myeloma increases nerve growth factor and other pain-related markers through interactions with the bone microenvironment

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Sam W. Z. Olechnowicz ◽  
Megan M. Weivoda ◽  
Seint T. Lwin ◽  
Szi K. Leung ◽  
Sarah Gooding ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Cell Activation ◽  
Cellular Interactions ◽  
Bone Microenvironment ◽  
Related Factors ◽  
Nerve Growth ◽  
Tnf Α

Abstract Interactions between multiple myeloma (MM) and bone marrow (BM) are well documented to support tumour growth, yet the cellular mechanisms underlying pain in MM are poorly understood. We have used in vivo murine models of MM to show significant induction of nerve growth factor (NGF) by the tumour-bearing bone microenvironment, alongside other known pain-related characteristics such as spinal glial cell activation and reduced locomotion. NGF was not expressed by MM cells, yet bone stromal cells such as osteoblasts expressed and upregulated NGF when cultured with MM cells, or MM-related factors such as TNF-α. Adiponectin is a known MM-suppressive BM-derived factor, and we show that TNF-α-mediated NGF induction is suppressed by adiponectin-directed therapeutics such as AdipoRON and L-4F, as well as NF-κB signalling inhibitor BMS-345541. Our study reveals a further mechanism by which cellular interactions within the tumour-bone microenvironment contribute to disease, by promoting pain-related properties, and suggests a novel direction for analgesic development.

In Vivo Induction and Delivery of Nerve Growth Factor, Using HEK-293 Cells

2004 ◽  
Vol 10 (9-10) ◽  
pp. 1492-1501 ◽  
Author(s):  
Michael P. McConnell ◽  
Sanjay Dhar ◽  
Sanjay Naran ◽  
Thang Nguyen ◽  
Ralph A. Bradshaw ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Nerve Growth ◽  
Hek 293 ◽  
Hek 293 Cells ◽  
293 Cells ◽  
In Vivo Induction

scholarly journals MicroRNA-98 reduces nerve growth factor expression in nicotine-induced airway remodeling

2020 ◽  
Vol 295 (52) ◽  
pp. 18051-18064
Author(s):  
Cherry Wongtrakool ◽  
Junsuk Ko ◽  
Andrew J. Jang ◽  
Kora Grooms ◽  
Sarah Chang ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Airway Remodeling ◽  
Luciferase Reporter ◽  
Mouse Lung ◽  
Luciferase Expression ◽  
Nerve Growth ◽  
Pparγ Agonist

Evolving evidence suggests that nicotine may contribute to impaired asthma control by stimulating expression of nerve growth factor (NGF), a neurotrophin associated with airway remodeling and airway hyperresponsiveness. We explored the hypothesis that nicotine increases NGF by reducing lung fibroblast (LF) microRNA-98 (miR-98) and PPARγ levels, thus promoting airway remodeling. Levels of NGF, miR-98, PPARγ, fibronectin 1 (FN1), endothelin-1 (EDN1, herein referred to as ET-1), and collagen (COL1A1 and COL3A1) were measured in human LFs isolated from smoking donors, in mouse primary LFs exposed to nicotine (50 μg/ml), and in whole lung homogenates from mice chronically exposed to nicotine (100 μg/ml) in the drinking water. In selected studies, these pathways were manipulated in LFs with miR-98 inhibitor (anti-miR-98), miR-98 overexpression (miR-98 mimic), or the PPARγ agonist rosiglitazone. Compared with unexposed controls, nicotine increased NGF, FN1, ET-1, COL1A1, and COL3A1 expression in human and mouse LFs and mouse lung homogenates. In contrast, nicotine reduced miR-98 levels in LFs in vitro and in lung homogenates in vivo. Treatment with anti-miR-98 alone was sufficient to recapitulate increases in NGF, FN1, and ET-1, whereas treatment with a miR-98 mimic significantly suppressed luciferase expression in cells transfected with a luciferase reporter linked to the putative seed sequence in the NGF 3′UTR and also abrogated nicotine-induced increases in NGF, FN1, and ET-1 in LFs. Similarly, rosiglitazone increased miR-98 and reversed nicotine-induced increases in NGF, FN1, and ET-1. Taken together, these findings demonstrate that nicotine-induced increases in NGF and other markers of airway remodeling are negatively regulated by miR-98.

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