scholarly journals Cytosolic GαsActs as an Intracellular Messenger to Increase Microtubule Dynamics and Promote Neurite Outgrowth

2009 ◽  
Vol 284 (16) ◽  
pp. 10462-10472 ◽  
Author(s):  
Jiang-Zhou Yu ◽  
Rahul H. Dave ◽  
John A. Allen ◽  
Tulika Sarma ◽  
Mark M. Rasenick
Keyword(s):  
Neurite Outgrowth ◽  
Microtubule Dynamics ◽  
Promote Neurite Outgrowth ◽  
Intracellular Messenger

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

Spastin Interacts with CRMP2 to Regulate Neurite Outgrowth by Controlling Microtubule Dynamics through Phosphorylation Modifications

2020 ◽  
Vol 19 ◽  
Author(s):  
Sumei Li ◽  
Jifeng Zhang ◽  
Jiaqi Zhang ◽  
Jiong Li ◽  
Longfei Cheng ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Hippocampal Neurons ◽  
Neuronal Development ◽  
Phosphorylation Site ◽  
Microtubule Dynamics ◽  
Microtubule Assembly ◽  
C Terminus ◽  
Mediator Protein ◽  
Branch Formation

Aims: Our work aims to revealing the underlying microtubule mechanism of neurites outgrowth during neuronal development, and also proposes a feasible intervention pathway for reconstructing neural network connections after nerve injury. Background: Microtubule polymerization and severing are the basis for the neurite outgrowth and branch formation. Collapsin response mediator protein 2 (CRMP2) regulates axonal growth and branching as a binding partner of the tubulin heterodimer to promote microtubule assembly. And spastin participates in the growth and regeneration of neurites by severing microtubules into small segments. However, how CRMP2 and spastin cooperate to regulate neurite outgrowth by controlling the microtubule dynamics needs to be elucidated. Objective: To explore whether neurite outgrowth was mediated by coordination of CRMP2 and spastin. Method: Hippocampal neurons were cultured in vitro in 24-well culture plates for 4 days before being used to perform the transfection. Calcium phosphate was used to transfect the CRMP2 and spastin constructs and their control into the neurons. An interaction between CRMP2 and spastin was examined by using pull down, CoIP and immunofluorescence colocalization assays. And immunostaining was also performed to determine the morphology of neurites. Result: We first demonstrated that CRMP2 interacted with spastin to promote the neurite outgrowth and branch formation. Furthermore, our results identified that phosphorylation modification failed to alter the binding affinities of CRMP2 for spastin, but inhibited their binding to microtubules. CRMP2 interacted with the MTBD domain of spastin via its C-terminus, and blocking the binding sites of them inhibited the outgrowth and branch formation of neurites. In addition, we confirmed one phosphorylation site S210 at spastin in hippocampal neurons and phosphorylation spastin at site S210 promoted the neurite outgrowth but not branch formation by remodeling microtubules. Conclusion: Taken together, our data demonstrated that the interaction of CRMP2 and spastin is required for neurite outgrowth and branch formation and their interaction is not regulated by their phosphorylation.

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.

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

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 RhoA-GTPase Modulates Neurite Outgrowth by Regulating the Expression of Spastin and p60-Katanin

Cells ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 230
Author(s):  
Dandan Tan ◽  
Haowen Zhang ◽  
Junyao Deng ◽  
Jingmin Liu ◽  
Jinkun Wen ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Signaling Pathway ◽  
Lentiviral Vector ◽  
Coiled Coil ◽  
Current Data ◽  
Microtubule Dynamics ◽  
Microtubule Severing ◽  
Downstream Effector ◽  
Rhoa Gtpase ◽  
Rhoa Signaling

RhoA-GTPase (RhoA) is widely regarded as a key molecular switch to inhibit neurite outgrowth by rigidifying the actin cytoskeleton. However, during neurite outgrowth, whether and how microtubule dynamics are regulated by RhoA remains to be elucidated. Herein, CT04 and Y27632 were used to inactivate RhoA and its downstream effector Rho-associated coiled coil-forming kinase (ROCK), while the RhoAQ63L lentiviral vector was utilized to overexpress the constitutively activated RhoA in dorsal root ganglion (DRG) neurons or neuronal differentiated PC12 cells. The current data illustrate that the RhoA signaling pathway negatively modulates neurite outgrowth and elevates the expression of Glu-tubulin (a marker for a stabilized microtubule). Meanwhile, the microtubule-severing proteins spastin and p60-katanin were downregulated by the RhoA signaling pathway. When spastin and p60-katanin were knocked down, the effects of RhoA inhibition on neurite outgrowth were significantly reversed. Taken together, this study demonstrates that the RhoA pathway-mediated inhibition of neurite outgrowth is not only related to the modulation of microfilament dynamics but is also attributable to the regulation of the expression of spastin and p60-katanin and thus influences microtubule dynamics.

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