Effects of nerve growth factor antagonist K252a on peritoneal mast cell degranulation: implications for rat postoperative ileus

2015 ◽  
Vol 309 (10) ◽  
pp. G801-G806 ◽  
Author(s):  
Sergio Berdún ◽  
Jakub Rychter ◽  
Patri Vergara
Keyword(s):  
Mast Cell ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Postoperative Ileus ◽  
Peritoneal Mast Cell ◽  
In Vivo Model ◽  
Dependent Manner ◽  
Nerve Growth

Stabilization of mast cell (MC) degranulation has been proposed to prevent postoperative ileus (POI). Nerve growth factor (NGF) mediates MC degranulation. The aim of the study was to evaluate whether NGF receptor antagonist K252a acts as a MC stabilizer in vitro and in vivo model of POI. Peritoneal mast cells (PMCs) were obtained from Sprague-Dawley rats and were incubated with K252a and exposed to NGF or Compound 48/80 (C48/80). MC degranulation was assessed by β-hexosaminidase assay. POI was induced in rats by intestinal manipulation (IM). Rats were pretreated with K252a (100 μg/kg sc) 20 min prior to POI induction. At 20 min after IM, release of rat mast cell protease 6 (RMCP-6) was evaluated in peritoneal lavage. At 24 h, intestinal transit (IT) and gastric emptying (GE) were evaluated. Ileal inflammation was assessed by myeloperoxidase (MPO) activity, expression of IL-6, NGF, TrkA, RMCP-2 and 6, and MC density within the full-thickness ileum. C48/80 and NGF evoked degranulation of PMCs in a dose-dependent manner. K252a prevented NGF-evoked, but not C48/80-evoked, MC degranulation. IM evoked the release of peritoneal RMCP-6 and subsequently delayed IT and GE. IM increased MPO activity and expression of IL-6. In IM rats, K252a prevented upregulation of IL-6 expression and reduced TrkA. IT, GE, and inflammation were not affected by K252a. K252a inhibited NGF-evoked degranulation of PMCs in vitro. In vivo, K252a decreased IL-6 and PMC degranulation. This may be of relevance for the development of new therapeutic targets for POI.

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 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.

scholarly journals Recombinant human nerve growth factor with a marked activity in vitro and in vivo

2005 ◽  
Vol 102 (51) ◽  
pp. 18658-18663 ◽  
Author(s):  
A. M. Colangelo ◽  
N. Finotti ◽  
M. Ceriani ◽  
L. Alberghina ◽  
E. Martegani ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Nerve Growth ◽  
Marked Activity ◽  
Human Nerve

Nerve growth factor does not influence the expression of β amyloid precursor protein mRNA in rat brain: in vivo and in vitro studies

1993 ◽  
Vol 620 (2) ◽  
pp. 292-296 ◽  
Author(s):  
Gianluigi Forloni ◽  
Roberto Del Bo ◽  
Nadia Angeretti ◽  
Simona Smiroldo ◽  
Nadia Gabellini ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Amyloid Precursor Protein ◽  
Rat Brain ◽  
Precursor Protein ◽  
In Vitro Studies ◽  
Nerve Growth ◽  
Β Amyloid

scholarly journals The Mixture of Gotu Kola, Cnidium Fruit, and Goji Berry Enhances Memory Functions by Inducing Nerve-Growth-Factor-Mediated Actions Both In Vitro and In Vivo

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1372
Author(s):  
Jin Gyu Choi ◽  
Zahra Khan ◽  
Seong Min Hong ◽  
Young Choong Kim ◽  
Myung Sook Oh ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Neuronal Cell ◽  
Main Role ◽  
Memory Functions ◽  
Nerve Growth ◽  
Goji Berry

Nerve growth factor (NGF), a typical neurotrophin, has been characterized by the regulation of neuronal cell differentiation and survival involved in learning and memory functions. NGF has a main role in neurite extension and synapse formation by activating the cyclic adenosine monophosphate-response-element-binding protein (CREB) in the hippocampus. The purpose of this study was to determine whether a mixture of Gotu Kola, Cnidium fruit, and Goji berry (KYJ) enhances memory function by inducing NGF-mediated actions both in vitro and in vivo. The KYJ combination increased NGF concentration and neurite length in C6 glioma and N2a neuronal cells, respectively. Additionally, we discovered memory-enhancing effects of KYJ through increased NGF-mediated synapse maturation, CREB phosphorylation, and cell differentiation in the mouse hippocampus. These findings suggest that this combination may be a potential nootropic cognitive enhancer via the induction of NGF and NGF-dependent activities.

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