Serum inducible kinase is a positive regulator of cortical dendrite development and is required for BDNF-promoted dendritic arborization

Guo, Shunling; Tan, Guangming; Li, Shuai; Cheng, Xuewen; Zhou, Yong‐Wu; Jia, Yunfang; Xiong, Hui; Tao, Jiong; Xiong, Zhi‐Qi

doi:10.1038/cr.2011.100

Cited by 13 publications

(16 citation statements)

References 56 publications

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“…30 SNK, can act as a polo-like kinase, when overexpressed can lead to abnormal branching into the significant process of the migrating cortical neurons in the electroporated cortices. 9 One study reported that glutamate stimulation could induce the activation of the SNK-SPAR pathway in cultured hippocampal neurons, resulting in a loss of mature dendritic spines. 11 In addition, a spleen-yin nourishing recipe-containing serum was also found having protective effects on neurons from the Abeta-induced neurotoxicity by blocking the SNK-SPAR pathway.…”

Section: Discussionmentioning

confidence: 99%

Retracted: Inhibition of SNK‐SPAR signaling pathway promotes the restoration of motor function in a rat model of ischemic stroke

Fan

Liu

Zhang

et al. 2017

J of Cellular Biochemistry

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This study aimed to investigate the effects of SPAR signaling pathway on the restoration of motor function in ischemic stroke (IS). Sprague-Dawley male rats were separated into the control and sham groups, as well as the group for middle cerebral artery occlusion (MCAO) model establishment. Successfully established rat ischemic models were randomly divided into model, SNK MCAO-del and pcDNA3.1-SNK groups. The evaluation of motor function among the rats in each group was assessed using a balance beam, a screen test and the Garcia scoring method. CatWalk gait analysis was employed to evaluate the effect of the SNK signaling pathway on rat motor function. Triphenyltetrazolium chloride (TTC) and TUNEL staining were techniques were utilized for cerebral infarction (CI) area as well for hippocampal neuron apoptosis. The quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting methods were performed to detect mRNA and protein expressions of SNK and SPAR. When compared with the model group, the SNK MCAO-del group displayed decreased motor function score and CI area, while contrasting results were observed in the pcDNA3.1-SNK group. According to the results obtained from the CatWalk gait analysis, the SNK MCAO-del group showed a clear improvement compared to the model group whereas the pcDNA3.1-SNK group exhibited poorer results than the model group in the objective parameters of the study, such as movement, speed, running duration, print area, maximal contact area, maximal, mean intensity, and stride length. These findings suggested that SNK gene silencing promotes motor function by inhibiting the SNK-SPAR signaling pathway in rats with ischemic stroke.

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Section: Discussionmentioning

confidence: 99%

Retracted: Inhibition of SNK‐SPAR signaling pathway promotes the restoration of motor function in a rat model of ischemic stroke

Fan

Liu

Zhang

et al. 2017

J of Cellular Biochemistry

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“…As such, MEK-ERK1/2 hyperactivity in the setting of TSC may promote dendritic hypertrophy via SRF-dependent transcriptional up-regulation of the FLNA gene. This is consistent with studies showing that MEK-ERK1/2 activity regulates neurite growth in many cell types ( e.g ., PC12 cells, many references) and dendritic growth in neurons (Collo et al, 2008; Guo et al, 2012; Ha and Redmond, 2008; Kim et al, 2004; Xu et al, 2014). Whatever the mechanism, our data showing that MEK1 overexpression leads to FLNA-dependent dendritic hypertrophy in wild type cells reinforces the finding that reduction of either MEK1 activity (using a dominant negative vector) or FLNA expression (using shRNA) normalizes dendritic hypertrophy in TSC.…”

Section: Discussionmentioning

confidence: 99%

MEK-ERK1/2-Dependent FLNA Overexpression Promotes Abnormal Dendritic Patterning in Tuberous Sclerosis Independent of mTOR

Zhang

Bartley

Gong

et al. 2014

Neuron

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Summary Abnormal dendritic complexity is a shared feature of many neurodevelopmental disorders associated with neurological defects. Here, we found that the actin-crosslinking protein filamin A (FLNA) is overexpressed in tuberous sclerosis complex (TSC) mice, a PI3K-mTOR model of neurodevelopmental disease that is associated with abnormal dendritic complexity. Both under-and overexpression of FLNA in wild-type neurons led to more complex dendritic arbors in vivo, suggesting that an optimal level of FLNA expression is required for normal dendritogenesis. In Tsc1null neurons, knocking down FLNA in vivo prevented dendritic abnormalities. Surprisingly, FLNA overexpression in Tsc1null neurons was dependent on MEK1/2 but not mTOR activity despite both pathways being hyperactive. In addition, increasing MEK-ERK1/2 activity led to dendritic abnormalities via FLNA and decreasing MEK-ERK1/2 signaling in Tsc1null neurons rescued dendritic defects. These data demonstrate that altered FLNA expression increases dendritic complexity and contributes to pathologic dendritic patterning in TSC in an mTOR-independent, ERK1/2-dependent manner.

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“…Activation of ERK signaling has been shown to regulate the expression –at the transcriptional level‐ of serum inducible kinase (SNK, also known as Polo‐like kinase 2 PLK2). In this study, the authors showed that SNK is required for BDNF‐induced dendritic but not axonal growth [Guo et al, ].…”

Section: Signaling Pathways Underlying Bdnf‐induced Dendritic and Axomentioning

confidence: 99%

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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Serum inducible kinase is a positive regulator of cortical dendrite development and is required for BDNF-promoted dendritic arborization

Cited by 13 publications

References 56 publications

Retracted: Inhibition of SNK‐SPAR signaling pathway promotes the restoration of motor function in a rat model of ischemic stroke

Retracted: Inhibition of SNK‐SPAR signaling pathway promotes the restoration of motor function in a rat model of ischemic stroke

MEK-ERK1/2-Dependent FLNA Overexpression Promotes Abnormal Dendritic Patterning in Tuberous Sclerosis Independent of mTOR

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

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