Guaifenesin Derivatives Promote Neurite Outgrowth and Protect Diabetic Mice from Neuropathy

2013 ◽  
Vol 56 (12) ◽  
pp. 5071-5078 ◽  
Author(s):  
Mallinath B. Hadimani ◽  
Meena K. Purohit ◽  
Chandrashaker Vanampally ◽  
Randy Van der Ploeg ◽  
Victor Arballo ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Diabetic Mice ◽  
Promote Neurite Outgrowth

scholarly journals Stimulation of neurite outgrowth in PC12 cells by EGF and KCl depolarization: a Ca(2+)-independent phenomenon.

1995 ◽  
Vol 130 (3) ◽  
pp. 701-710 ◽  
Author(s):  
M D Mark ◽  
Y Liu ◽  
S T Wong ◽  
T R Hinds ◽  
D R Storm
Keyword(s):  
Map Kinase ◽  
Neurite Outgrowth ◽  
Pc12 Cells ◽  
Kinase Activity ◽  
Neurite Growth ◽  
Intracellular Camp ◽  
Regulation Of Transcription ◽  
Promote Neurite Outgrowth ◽  
Synergistic Regulation ◽  
Stimulation Of

MAP kinase activity is necessary for growth factor induction of neurite outgrowth in PC12 cells. Although NGF and EGF both stimulate MAP kinase activity, EGF does not stimulate neurite extension. We report that EGF, in combination with KCl, stimulates neurite outgrowth in PC12 cells. This phenomenon was independent of intracellular Ca2+ increases and not due to enhancement of MAP kinase activity over that seen with EGF alone. However, EGF plus KCl increased intracellular cAMP, and other cAMP elevating agents acted synergistically with EGF to promote neurite outgrowth. Stimulation of neurite outgrowth by cAMP and EGF was blocked by inhibitors of transcription suggesting that synergistic regulation of transcription by the cAMP and MAP kinase pathways may stimulate neurite growth.

Spastin Interacts with CRMP5 to Promote Neurite Outgrowth by Controlling the Microtubule Dynamics

2018 ◽  
Vol 78 (12) ◽  
pp. 1191-1205 ◽  
Author(s):  
Zhisheng Ji ◽  
Guowei Zhang ◽  
Li Chen ◽  
Jiong Li ◽  
Yuhao Yang ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Microtubule Dynamics ◽  
Promote Neurite Outgrowth

Overexpression of nerve growth factor in peritoneal fluid from women with endometriosis may promote neurite outgrowth in endometriotic lesions

2011 ◽  
Vol 95 (3) ◽  
pp. 1123-1126 ◽  
Author(s):  
Maria Luisa Barcena de Arellano ◽  
Julia Arnold ◽  
Filiberto Vercellino ◽  
Vito Chiantera ◽  
Achim Schneider ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Neurite Outgrowth ◽  
Peritoneal Fluid ◽  
Nerve Growth ◽  
Promote Neurite Outgrowth

scholarly journals Calcium influx into neurons can solely account for cell contact-dependent neurite outgrowth stimulated by transfected L1.

1992 ◽  
Vol 119 (4) ◽  
pp. 883-892 ◽  
Author(s):  
E J Williams ◽  
P Doherty ◽  
G Turner ◽  
R A Reid ◽  
J J Hemperly ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Pc12 Cells ◽  
Calcium Influx ◽  
Polysialic Acid ◽  
Cell Contact ◽  
3T3 Cells ◽  
Cerebellar Neurons ◽  
Calcium Dependent ◽  
Promote Neurite Outgrowth ◽  
Neural Cell Adhesion

We have used monolayers of control 3T3 cells and 3T3 cells expressing transfected human L1 as a culture substrate for rat PC12 cells and rat cerebellar neurons. PC12 cells and cerebellar neurons extended longer neurites on human L1 expressing cells. Neurons isolated from the cerebellum at postnatal day 9 responded equally as well as those isolated at postnatal day 1-4, and this contrasts with the failure of these older neurons to respond to the transfected human neural cell adhesion molecule (NCAM). Human L1-dependent neurite outgrowth could be blocked by antibodies that bound to rat L1 and, additionally, the response could be fully inhibited by pertussis toxin and substantially inhibited by antagonists of L- and N-type calcium channels. Calcium influx into neurons induced by K+ depolarization fully mimics the L1 response. Furthermore, we show that L1- and K+(-)dependent neurite outgrowth can be specifically inhibited by a reduction in extracellular calcium to 0.25 microM, and by pretreatment of cerebellar neurons with the intracellular calcium chelator BAPTA/AM. In contrast, the response was not inhibited by heparin or by removal of polysialic acid from neuronal NCAM both of which substantially inhibit NCAM-dependent neurite outgrowth. These data demonstrate that whereas NCAM and L1 promote neurite outgrowth via activation of a common CAM-specific second messenger pathway in neurons, neuronal responsiveness to NCAM and L1 is not coordinately regulated via posttranslational processing of NCAM. The fact that NCAM- and L1-dependent neurite outgrowth, but not adhesion, are calcium dependent provides further evidence that adhesion per se does not directly contribute to neurite outgrowth.

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