SH2B1β enhances fibroblast growth factor 1 (FGF1)-induced neurite outgrowth through MEK-ERK1/2-STAT3-Egr1 pathway

Lin, Wei-Fan; Chen, Chien-Jen; Chang, Yu‐Jung; Chen, Suliang; Chiu, Ing‐Ming; Chen, Linyi

doi:10.1016/j.cellsig.2009.02.009

Cited by 43 publications

(51 citation statements)

References 70 publications

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“…We excluded NGF-dependent induction of MGL transcription by quantitative PCR (Fig. 4B), using early growth response protein (Egr)1 as positive control (22) (Fig. 4B 1 ; see Fig.…”

Section: Resultsmentioning

confidence: 99%

Nerve growth factor scales endocannabinoid signaling by regulating monoacylglycerol lipase turnover in developing cholinergic neurons

Keimpema

Tortoriello

Alpár

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Endocannabinoid, particularly 2-arachidonoyl glycerol (2-AG), signaling has recently emerged as a molecular determinant of neuronal migration and synapse formation during cortical development. However, the cell type specificity and molecular regulation of spatially and temporally confined morphogenic 2-AG signals remain unexplored. Here, we demonstrate that genetic and pharmacological manipulation of CB 1 cannabinoid receptors permanently alters cholinergic projection neuron identity and hippocampal innervation. We show that nerve growth factor (NGF), implicated in the morphogenesis and survival of cholinergic projection neurons, dose-dependently and coordinately regulates the molecular machinery for 2-AG signaling via tropomyosine kinase A receptors in vitro. In doing so, NGF limits the sorting of monoacylglycerol lipase (MGL), rate limiting 2-AG bioavailability, to proximal neurites, allowing cell-autonomous 2-AG signaling at CB 1 cannabinoid receptors to persist at atypical locations to induce superfluous neurite extension. We find that NGF controls MGL degradation in vitro and in vivo and identify the E3 ubiquitin ligase activity of breast cancer type 1 susceptibility protein (BRCA1) as a candidate facilitating MGL's elimination from motile neurite segments, including growth cones. BRCA1 inactivation by cisplatin or genetically can rescue and reposition MGL, arresting NGF-induced growth responses. These data indicate that NGF can orchestrate endocannabinoid signaling to promote cholinergic differentiation and implicate BRCA1 in determining neuronal morphology.axon guidance | basal forebrain | neurotrophin | protein stability | choline acetyltransferase C B 1 cannabinoid receptors (CB 1 Rs) are the targets of marijuana (Cannabis spp.)-derived phytocannabinoids and endocannabinoids, including 2-arachidonoyl glycerol (2-AG) (1). 2-AG liberated from postsynaptic neurons serves as a retrograde messenger to limit neurotransmitter release from many mature presynapses (1). However, 2-AG signaling also emerges as a molecular determinant of cortical development (2-4). Despite recent advances, the contribution of endocannabinoids (specifically 2-AG) to neuronal diversification and the development of synaptic connectivity in subcortical territories remains unknown. Cholinergic projection neurons within a continuum of magnocellular nuclei in the basal forebrain (5) are appealing candidates for developmental 2-AG actions considering their CB 1 R expression (1) and the endocannabinoid sensitivity of acetylcholine release in adulthood (6).Cholinergic afferents innervating the cerebral cortex are essential for learning and memory (5, 7). A favored approach to rescue cholinergic neurotransmission under disease conditions relies on neurotrophins to maintain the molecular identity, synaptic signaling, and survival of cholinergic neurons (8, 9). Nerve growth factor (NGF) appears particularly efficacious to promote the phenotypic differentiation and synaptic connectivity of postnatal cholinergic projection neurons (9, 10), as ill...

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“…We excluded NGF-dependent induction of MGL transcription by quantitative PCR (Fig. 4B), using early growth response protein (Egr)1 as positive control (22) (Fig. 4B 1 ; see Fig.…”

Section: Resultsmentioning

confidence: 99%

Nerve growth factor scales endocannabinoid signaling by regulating monoacylglycerol lipase turnover in developing cholinergic neurons

Keimpema

Tortoriello

Alpár

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…The difference in cellular response to NPY in adipocyte precursor cells between the white and brown adipose tissues may be simply due to the different characteristics of these cells which expressing different genes. previously [15,17,22,24,39].…”

Section: Discussionmentioning

confidence: 99%

“…As shown in Figure 4, treatment of cells with NPY (30 nM and 100 n) induced the phosphorylation, indicating that functional NPY receptor was present in SVC. We further examined STAT3 phosphorylation at Ser727 and Tyr705, as the serine residue of STAT3 is known to be a downstream target of the ERK pathway [15,17,22,24,39]. NPY treatment at the concentration of 30 nM or higher induced the Ser phosphorylation, but not the Tyr phosphorylation (Fig.…”

mentioning

confidence: 99%

Neuropeptide Y activates phosphorylation of ERK and STAT3 in stromal vascular cells from brown adipose tissue, but fails to affect thermogenic function of brown adipocytes

et al. 2012

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“…phosphorylation of STAT3 [pSTAT3(S727)] and expression of the STAT3 target gene Egr1 during neuronal differentiation (24). We set out to determine whether SH2B1␤ binds to STAT3, and if it does, which domain(s) is responsible for the interaction.…”

Section: Resultsmentioning

confidence: 99%

“…SH2B1␤ (␤ variant of SH2B1) participates in signaling pathways for several receptor tyrosine kinases (RTKs), such as insulin, NGF (1), glial cell line-derived neurotrophic factor (GDNF), FGF1, and erythropoietin receptors (18)(19)(20)(21)(22)(23). We have previously shown that SH2B1␤ enhances FGF1-induced neurite outgrowth in PC12 cells, mainly through the MAPK kinase (MEK)-extracellular signal-regulated kinase (ERK1/2)-STAT3 pathway and the expression of STAT3 target gene Egr1 (24). SH2B1␤ also undergoes nucleocytoplasmic shuttling and regulates a subset of NGF-responsive genes, suggestive of its involvement in transcriptional regulation (25,26).…”

mentioning

confidence: 99%

SH2B1β Interacts with STAT3 and Enhances Fibroblast Growth Factor 1-Induced Gene Expression during Neuronal Differentiation

Chang

Chen

et al. 2014

Molecular and Cellular Biology

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SH2B1β enhances fibroblast growth factor 1 (FGF1)-induced neurite outgrowth through MEK-ERK1/2-STAT3-Egr1 pathway

Cited by 43 publications

References 70 publications

Nerve growth factor scales endocannabinoid signaling by regulating monoacylglycerol lipase turnover in developing cholinergic neurons

Nerve growth factor scales endocannabinoid signaling by regulating monoacylglycerol lipase turnover in developing cholinergic neurons

Neuropeptide Y activates phosphorylation of ERK and STAT3 in stromal vascular cells from brown adipose tissue, but fails to affect thermogenic function of brown adipocytes

SH2B1β Interacts with STAT3 and Enhances Fibroblast Growth Factor 1-Induced Gene Expression during Neuronal Differentiation

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