LIM Kinase 1 (LIMK1) Interacts with Tropomyosin-related Kinase B (TrkB) and Mediates Brain-derived Neurotrophic Factor (BDNF)-induced Axonal Elongation

Dong, Qing; Ji, Yun-Song; Cai, Chonghai; Chen, Zhe-Yu

doi:10.1074/jbc.m112.405415

Cited by 30 publications

(33 citation statements)

References 47 publications

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“…The growth cone is composed of microtubules and filamentous actin (F-actin), and the actin cytoskeleton is the motivating force for growth cones, and thus F-actin plays a major part in neuronal growth. LIM kinases regulate the structure of the actin cytoskeleton by phosphorylation and inactivation of the actin depolymerization factor cofilin, and activity of LIM kinase is regulated by Rho-GTPase Rac1 [19,20,54]. A growing body of evidence showed that MAPK is related to the cytoskeleton [20], but the mechanism is unclear.…”

Section: Discussionmentioning

confidence: 99%

“…LIM kinases regulate the structure of the actin cytoskeleton by phosphorylation and inactivation of the actin depolymerization factor cofilin, and activity of LIM kinase is regulated by Rho-GTPase Rac1 [19,20,54]. A growing body of evidence showed that MAPK is related to the cytoskeleton [20], but the mechanism is unclear. Based on this, we propose that Mst3b interacts with Rac1 in modulating the F-actin cytoskeleton.…”

Section: Discussionmentioning

confidence: 99%

“…After concentration, total protein was detected using the BCA method (Beyotime, China), and protein extracts were boiled with SDS sample buffer (Beyotime). Western blotting analysis was carried out as described previously [20]. Briefly, 25 μg of protein was subjected to SDS-PAGE and electro-transferred to PVDF membranes.…”

Section: Adv Infection and Western Blotting Analysismentioning

confidence: 99%

“…Growth cone motility and protrusion of the leading edge membrane depend on the dynamic properties of actin, a central part of the mechanism that controls growth cone exploration [35,36]. Cofilin regulates actin organization by virtue of its primary activity: increasing actin turnover and restoring retrograde flow to reorganize the actin superstructures [20,37]. Thus, we want to observe the small G protein Rac1 to see whether it is modulated by Mst3b.…”

Section: Mst3b Modulate Actin Skeleton By Regulating the Limk/cofilinmentioning

confidence: 99%

“…F-actin, an essential component of growth cones, is a motivating factor for neuronal growth, playing a particularly important part in promoting neuron regrowth through the regulation of Rac1/LIMK1/Cofilin [19,20]. Rac1 is a homolog of Ras; therefore, we hypothesized that Mst3b also links to Rac1 and stimulates LIMK/Cofilin activation.…”

Section: Introductionmentioning

confidence: 99%

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Mst3b Promotes Spinal Cord Neuronal Regeneration by Promoting Growth Cone Branching Out in Spinal Cord Injury Rats

Zhang

Tian

et al. 2014

Mol Neurobiol

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Spinal cord injury is a severe clinical problem, and research searching activity molecular that can promote spinal cord injury repairing is very prevalent. Mst3b can promote repair of damaged peripheral nerves and the optic nerve, but has been rarely reported in spinal cord injury research. Through detecting its expression in different periods of injured spinal cord, we found that the expression of Mst3b was significantly upregulated in injured spinal cord neurons. Increasing Mst3b expression using adenovirus in vivo and in vitro promoted axonal regeneration of spinal cord neurons, which led to behavioral and electrophysiological improvement. Downregulation of Mst3b level had the adverse effects. Increasing Mst3b expression in PC12 cells resulted in an elevation of P42/44(MAPK) and LIMK/Cofilin activation. These results identified Mst3b as a powerful regulator for promoting spinal cord injury recovery through the P42/44(MAPK) and LIMK/Cofilin signaling pathways.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Adv Infection and Western Blotting Analysismentioning

confidence: 99%

Section: Mst3b Modulate Actin Skeleton By Regulating the Limk/cofilinmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Mst3b Promotes Spinal Cord Neuronal Regeneration by Promoting Growth Cone Branching Out in Spinal Cord Injury Rats

Zhang

Tian

et al. 2014

Mol Neurobiol

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Dysregulation of LIMK‐1/cofilin‐1 pathway: A possible basis for alteration of neuronal morphology in experimental cerebral malaria

Kumar

Malwade

Vanka

et al. 2017

Annals of Neurology

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Cellular and molecular mechanisms regulating neuronal growth by brain‐derived neurotrophic factor

et al. 2016

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Brain-derived neurotrophic factor (BDNF) and its receptors TrkB and p75 regulate dendritic and axonal growth during development and maintenance of the mature nervous system; however, the cellular and molecular mechanisms underlying this process are not fully understood. In recent years, several advances have shed new light on the processes behind the regulation of BDNF-mediated structural plasticity including control of neuronal transcription, local translation of proteins, and regulation of cytoskeleton and membrane dynamics. In this review, we summarize recent advances in the field of BDNF signaling in neurons to induce neuronal growth. V C 2016 Wiley Periodicals, Inc.Key Words: BDNF; dendritic growth; signaling; cytoskeleton dynamics; membrane trafficking Introduction T he functionality of the nervous system (NS) depends on the extent of connectivity achieved by neurons. Although there is wide range of neuronal morphologies, neurons are specialized to form part of a given neuronal circuit and thus their morphology must adjust to this task [Gao, 2007]. In this regard, neurons are highly polarized cells composed of two main domains: the somato-dendritic compartment where neurons receive and integrate information from several axonal inputs and axons that are responsible for transmitting the action potential and conveying the information to the next relay in the network. A close relationship between the appropriate development of dendrites and axons and the functionality of the NS has been described. For example, alterations in dendrites, axonal inputs and dendritic spines are linked to neurodevelopmental and neuropathological conditions. Thus, the study of the mechanisms implicated in the regulation of neuronal morphology during development and maintenance of the adult NS is a focus of intense research [Armstrong et al., 1998;Wood et al., 2004;Bronfman et al., 2007;Dickstein et al., 2010;Cabeza et al., 2012;Eiland and McEwen, 2012;Kulkarni and Firestein, 2012].Neuronal morphology is regulated by both intrinsic and extrinsic factors, whose actions are overlapping. The intrinsic factors are described as the action of the genetic program of neurons that leads to a basic pattern of branching. In addition to this, there is an extensive list of molecules grouped as extrinsic factors that shape axonal and dendritic morphology throughout development and in response to sensory experience. These include bone morphogenetic family proteins (BMPs), semaphorins, Reelin, neurotrophins, and neuronal activity, among others [Jan and Jan, 2010]. The mechanisms underlying the effects of external cues to induce dendritic and axonal branching have only begun to be understood, and several steps including stimulation of intracellular signaling pathways to activate specific transcription factors, local synthesis of proteins and cellular membrane addition and turnover are involved. An interesting point of convergence is the effect of these external signals on the stability and dynamics of the cytoskeleton and the activity of molecular mo...

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LIM Kinase 1 (LIMK1) Interacts with Tropomyosin-related Kinase B (TrkB) and Mediates Brain-derived Neurotrophic Factor (BDNF)-induced Axonal Elongation

Cited by 30 publications

References 47 publications

Mst3b Promotes Spinal Cord Neuronal Regeneration by Promoting Growth Cone Branching Out in Spinal Cord Injury Rats

Mst3b Promotes Spinal Cord Neuronal Regeneration by Promoting Growth Cone Branching Out in Spinal Cord Injury Rats

Dysregulation of LIMK‐1/cofilin‐1 pathway: A possible basis for alteration of neuronal morphology in experimental cerebral malaria

Cellular and molecular mechanisms regulating neuronal growth by brain‐derived neurotrophic factor

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