Dose-Dependent Effect of Nerve Growth Factor Mimetic GK-2 in a Wistar Rat Diabetes Model

2021 ◽  
Author(s):  
S. V. Ivanov ◽  
R. U. Ostrovskaya ◽  
T. A. Gudasheva ◽  
S. B. Seredenin
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Wistar Rat ◽  
Dependent Effect ◽  
Nerve Growth ◽  
Diabetes Model ◽  
Dose Dependent ◽  
Dose Dependent Effect

scholarly journals Nerve growth factor action is mediated by cyclic AMP- and Ca+2/phospholipid-dependent protein kinases.

1986 ◽  
Vol 103 (3) ◽  
pp. 887-893 ◽  
Author(s):  
J Cremins ◽  
J A Wagner ◽  
S Halegoua
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Tyrosine Hydroxylase ◽  
Protein Kinase ◽  
Enzyme Activation ◽  
Dependent Protein Kinase ◽  
Nerve Growth ◽  
Camp Dependent Protein Kinase ◽  
Dependent Protein ◽  
Dose Dependent

Nerve growth factor (NGF) mediates the phosphorylation of tyrosine hydroxylase in PC12 cells on two distinct peptide fragments, separable by two-dimensional tryptic phosphopeptide mapping (phosphopeptides T1 and T3). Phorbol diester derivatives capable of activating Ca+2/phospholipid-dependent protein kinase (C-kinase) cause a specific phosphorylation of peptide T3 in a dose-dependent, saturable manner. Derivatives of the endogenous C-kinase activator diacylglycerol, also cause the phosphorylation of tyrosine hydroxylase on peptide T3. The C-kinase inhibitors chlorpromazine and trifluoperazine inhibit the phorbol diester stimulated phosphorylation of site T3 in a dose-dependent manner. These agents inhibit the phosphorylation of T3 in response to NGF, but have no effect on NGF's ability to cause T1 phosphorylation. In a PC12 mutant deficient in cAMP-dependent protein kinase activity, NGF mediates the phosphorylation of tyrosine hydroxylase on peptide T3 but not on T1. We conclude that NGF mediates the activation of both the cAMP-dependent protein kinase and the C-kinase to phosphorylate substrate proteins. These kinases can act independently to phosphorylate tyrosine hydroxylase, each at a different site, and each of which results in the enzyme activation. A molecular framework is thus provided for events underlying NGF action.

scholarly journals 2.5S nerve growth factor enhances survival, phagocytosis, and superoxide production of murine neutrophils

Blood ◽  
1991 ◽  
Vol 77 (6) ◽  
pp. 1320-1325 ◽  
Author(s):  
Y Kannan ◽  
H Ushio ◽  
H Koyama ◽  
M Okada ◽  
M Oikawa ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Peripheral Blood ◽  
Superoxide Production ◽  
Colony Stimulating Factor ◽  
Nerve Growth ◽  
Zymosan A ◽  
Inflammatory Processes ◽  
Dose Dependent ◽  
Stimulating Factor

The effect of 2.5S nerve growth factor (NGF) on survival, phagocytosis, and superoxide production of murine neutrophils was examined and compared with the effects of interleukin-3 (IL-3) and recombinant GM colony-stimulating factor (rGM-CSF). NGF enhanced the viability of neutrophils isolated from peripheral blood and peritoneal cavity in a dose-dependent way. IL-3 50 U/mL had no effect. rGM-CSF 50 U/mL had an effect similar to that of 50 ng/mL NGF. NGF also enhanced the phagocytosis of hydrophilic microspheres by peritoneal neutrophils, and the activity of NGF was greater than that of IL-3 or rGM-CSF. NGF enhanced the superoxide production induced by phorbol 12-myristate 13- acetate (PMA), which acts at postreceptor sites, and that induced by opsonized zymosan, a receptor-mediated ligand. The stimulating activity of NGF was largely comparable to that of rGM-CSF. The present data show that NGF bound to neutrophils enhances their survival, phagocytosis, and superoxide production. Thus, we postulate that NGF plays an important role in the inflammatory processes.

scholarly journals 2.5S nerve growth factor enhances survival, phagocytosis, and superoxide production of murine neutrophils

Blood ◽  
1991 ◽  
Vol 77 (6) ◽  
pp. 1320-1325 ◽  
Author(s):  
Y Kannan ◽  
H Ushio ◽  
H Koyama ◽  
M Okada ◽  
M Oikawa ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Peripheral Blood ◽  
Superoxide Production ◽  
Colony Stimulating Factor ◽  
Nerve Growth ◽  
Zymosan A ◽  
Inflammatory Processes ◽  
Dose Dependent ◽  
Stimulating Factor

Abstract The effect of 2.5S nerve growth factor (NGF) on survival, phagocytosis, and superoxide production of murine neutrophils was examined and compared with the effects of interleukin-3 (IL-3) and recombinant GM colony-stimulating factor (rGM-CSF). NGF enhanced the viability of neutrophils isolated from peripheral blood and peritoneal cavity in a dose-dependent way. IL-3 50 U/mL had no effect. rGM-CSF 50 U/mL had an effect similar to that of 50 ng/mL NGF. NGF also enhanced the phagocytosis of hydrophilic microspheres by peritoneal neutrophils, and the activity of NGF was greater than that of IL-3 or rGM-CSF. NGF enhanced the superoxide production induced by phorbol 12-myristate 13- acetate (PMA), which acts at postreceptor sites, and that induced by opsonized zymosan, a receptor-mediated ligand. The stimulating activity of NGF was largely comparable to that of rGM-CSF. The present data show that NGF bound to neutrophils enhances their survival, phagocytosis, and superoxide production. Thus, we postulate that NGF plays an important role in the inflammatory processes.

Dose-dependent responses to nerve growth factor by adult rat cholinergic medial septum and neostriatum neurons

1991 ◽  
Vol 552 (2) ◽  
pp. 320-329 ◽  
Author(s):  
H. Lee Vahlsing ◽  
Theo Hagg ◽  
Michael Spencer ◽  
James M. Conner ◽  
Marston Manthorpe ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Medial Septum ◽  
Nerve Growth ◽  
Adult Rat ◽  
Dose Dependent

Hypotension induced by intravascular administration of nerve growth factor in the rat

1991 ◽  
Vol 80 (6) ◽  
pp. 565-569 ◽  
Author(s):  
Q. Yan ◽  
S. L. Settle ◽  
M. R. Wilkins
Keyword(s):  
Blood Pressure ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Area Postrema ◽  
Femoral Vein ◽  
Growth Factor Receptor ◽  
Nerve Growth ◽  
Vasoactive Substances ◽  
High Level ◽  
Dose Dependent

1. The observation that the area postrema expresses a high level of nerve-growth-factor-receptor immunoreactivity prompted an investigation of the effects of nerve growth factor on autonomic function in the rat. 2. Bolus injection of pharmacological doses of the peptide via the femoral vein led to reproducible, dose-dependent falls in blood pressure. 3. Administration via the vertebral artery, a more direct route to the brainstem, did not appear to lower the threshold dose required to induce hypotension. Furthermore, pretreatment with hexamethonium did not inhibit the hypotensive response to nerve growth factor. 4. Administration of a second dose of nerve growth factor after recovery from the first injection produced little or no fall in blood pressure. Similarly, pretreatment with the mast cell degranulating agent, compound 48/80, rendered the animal refractory to nerve growth factor. 5. The fall in blood pressure induced by nerve growth factor was markedly attenuated by pretreatment with chlorpheniramine. 6. It is concluded that the fall in blood pressure induced by intravenous administration of pharmacological doses of nerve growth factor is mediated by vasoactive substances, particularly histamine, released from mast cells.

scholarly journals Functional properties of murine macrophages promoted by nerve growth factor

Blood ◽  
1996 ◽  
Vol 88 (12) ◽  
pp. 4630-4637 ◽  
Author(s):  
Y Susaki ◽  
S Shimizu ◽  
K Katakura ◽  
N Watanabe ◽  
K Kawamoto ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Kinase Inhibitor ◽  
Flow Cytometric Analysis ◽  
Peritoneal Macrophages ◽  
Dependent Manner ◽  
Recombinant Interferon ◽  
Nerve Growth ◽  
Murine Macrophages ◽  
Dose Dependent

The stimulating effect of nerve growth factor (NGF) on phagocytosis, parasite killing, and interleukin-1beta (IL-1beta) production of murine peritoneal macrophages was assessed. In the presence of various doses of NGF, macrophages showed the increased phagocytosis of both nonspecific hydrophilic microspheres and sheep red blood cells (SRBC) opsonized with anti-SRBC antibodies (Ab) or complement in a dose-dependent manner. NGF also enhanced killing of Leishmania donovani promastigotes by macrophages, and its ability was comparable with that of an optimal dose of recombinant granulocyte-macrophage colony-stimulating factor or recombinant interferon-gamma. The addition of NGF to peritoneal macrophages and monocyte-macrophage J774A.1 cells led to a significant release of IL-1beta in a dose-dependent manner and expression of IL-1beta mRNA. Because pretreatment of peritoneal macrophages and J774A.1 cells with K-252a, a tyrosine kinase inhibitor, completely suppressed these NGF-mediated stimulating effects and p140trk phosphorylation and because flow cytometric analysis with specific Ab against two distinct NGF receptors showed the expression of p140trk, unlike p75LNGFR, on the surface of macrophages, the stimulating activity of NGF to murine macrophages may be mediated through p140trk. Thus, NGF may act as an activator for murine macrophages in the process of inflammatory and immune actions.

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