SmgGDS antagonizes BPGAP1-induced Ras/ERK activation and neuritogenesis in PC12 cell differentiation

Ravichandran, Aarthi; Low, Boon Chuan

doi:10.1091/mbc.e12-04-0300

Cited by 14 publications

(11 citation statements)

References 39 publications

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“…NGFβ binds to two different receptors: the TrkA tyrosine kinase receptor with high affinity and the p75 NTR with low affinity [32]. In PC12 cells, NGFβ activates the ERK signal through the TrkA, that leading to neurite outgrowth [33]. In the present study, we confirmed the NGFβ activities, whereas SPARC alone did not change the phosphorylated state of ERK1/2 and subsequent neuritogenesis.…”

Section: Discussionsupporting

confidence: 75%

Interaction of Nerve Growth Factor β with Adiponectin and SPARC Oppositely Modulates its Biological Activity

Okura

Imao

Murashima

et al. 2019

IJMS

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Both adiponectin and secreted protein, acidic and rich in cysteine (SPARC) inhibit platelet-derived growth factor-BB (PDGF-BB)-induced and basic fibroblast growth factor (FGF2)-induced angiogenic activities through direct and indirect interactions. Although SPARC enhances nerve growth factor (NGF)-dependent neurogenesis, the physical interaction of NGFβ with adiponectin and SPARC remains obscure. Therefore, we first examined their intermolecular interaction by surface plasmon resonance method. NGFβ bound to immobilized SPARC with the binding constant of 59.4 nM, comparable with that of PDGF-BB (24.5 nM) but far less than that of FGF2 (14.4 µM). NGFβ bound to immobilized full length adiponectin with the binding constant of 103 nM, slightly higher than those of PDGF-BB (24.3 nM) and FGF2 (80.2 nM), respectively. Treatment of PC12 cells with SPARC did not cause mitogen-activated protein kinase (MAPK) activation and neurite outgrowth. However, simultaneous addition of SPARC with NGFβ enhanced NGFβ-induced MAPK phosphorylation and neurite outgrowth. Treatment of the cells with adiponectin increased AMP-activated protein kinase (AMPK) phosphorylation but failed to induce neurite outgrowth. Simultaneous treatment with NGFβ and adiponectin significantly reduced cell size and the number of cells with neurite, even after silencing the adiponectin receptors by their siRNA. These results indicate that NGFβ directly interacts with adiponectin and SPARC, whereas these interactions oppositely regulate NGFβ functions.

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Section: Discussionsupporting

confidence: 75%

Interaction of Nerve Growth Factor β with Adiponectin and SPARC Oppositely Modulates its Biological Activity

Okura

Imao

Murashima

et al. 2019

IJMS

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“…An interesting protein in this context is SmgGDS, which associates with the active and inactive forms of Rac1 , being sequestered in the nucleus together with Rac1 . Its function in neurons appears to be related to neurite outgrowth in physiological conditions . Rac1 function is also very well controlled as for example by TIAM‐1 and Trio, two GEFs able to activate Rac1 .…”

Section: Introductionmentioning

confidence: 99%

Neuronal Rho GTPase Rac1 elimination confers neuroprotection in a mouse model of permanent ischemic stroke

et al. 2017

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The Rho GTPase Rac1 is a multifunctional protein involved in distinct pathways ranging from development to pathology. The aim of the present study was to unravel the contribution of neuronal Rac1 in regulating the response to brain injury induced by permanent focal cerebral ischemia (pMCAO). Our results show that pMCAO significantly increased total Rac1 levels in wild type mice, mainly through rising nuclear Rac1, while a reduction in Rac1 activation was observed. Such changes preceded cell death induced by excitotoxic stress. Pharmacological inhibition of Rac1 in primary neuronal cortical cells prevented the increase in oxidative stress induced after overactivation of glutamate receptors. However, this was not sufficient to prevent the associated neuronal cell death. In contrast, RNAi-mediated knock down of Rac1 in primary cortical neurons prevented cell death elicited by glutamate excitotoxicity and decreased the activity of NADPH oxidase. To test whether in vivo down regulation of neuronal Rac1 was neuroprotective after pMCAO, we used tamoxifen-inducible neuron-specific conditional Rac1-knockout mice. We observed a significant 50% decrease in brain infarct volume of knockout mice and a concomitant increase in HIF-1α expression compared to littermate control mice, demonstrating that ablation of Rac1 in neurons is neuroprotective. Transmission electron microscopy performed in the ischemic brain showed that lysosomes in the infarct of Rac1- knockout mice were preserved at similar levels to those of non-infarcted tissue, while littermate mice displayed a decrease in the number of lysosomes, further corroborating the notion that Rac1 ablation in neurons is neuroprotective. Our results demonstrate that Rac1 plays important roles in the ischemic pathological cascade and that modulation of its levels is of therapeutic interest.

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“…We recently established the roles of the BCH domain in modulating a variety of cellular events ( Pan and Low, 2012 ; Ravichandran and Low, 2013 ). Of interest, these BCH domain–containing proteins display distinct subcellular localizations.…”

Section: Discussionmentioning

confidence: 99%

KIF5B transports BNIP-2 to regulate p38 mitogen-activated protein kinase activation and myoblast differentiation

Peng

Chew

Zhang

et al. 2015

MBoC

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SmgGDS antagonizes BPGAP1-induced Ras/ERK activation and neuritogenesis in PC12 cell differentiation

Cited by 14 publications

References 39 publications

Interaction of Nerve Growth Factor β with Adiponectin and SPARC Oppositely Modulates its Biological Activity

Interaction of Nerve Growth Factor β with Adiponectin and SPARC Oppositely Modulates its Biological Activity

Neuronal Rho GTPase Rac1 elimination confers neuroprotection in a mouse model of permanent ischemic stroke

KIF5B transports BNIP-2 to regulate p38 mitogen-activated protein kinase activation and myoblast differentiation

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