Nerve Growth Factor Regulates Adrenergic Expression

Tai, T.C.; Wong-Faull, David C.; Claycomb, Robert; Wong, Dona L.

doi:10.1124/mol.106.026237

Cited by 8 publications

(12 citation statements)

References 57 publications

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“…Indeed, EGR1 was dramatically recruited into the nucleus when induced by NGF in PC12 cells, as demonstrated by Western blot analysis ( Figure 1D) and EMSA (Supplementary Figure S1 at http://www.BiochemJ.org/bj/440/bj4400273add.htm). These results are consistent with those reported previously [33]. Thus we deduced that the NGF induction of heparanase in PC12 cells was likely to be mediated by the TrkA-EGR1 pathway.…”

Section: Ngf-induced Heparanase Expression In Pc12 Cells Is Attenuatesupporting

confidence: 93%

“…Nuclear extracts (NE) isolated from PC-12 cells exposed to NGF for 60 and 120 min were subjected to EMSA using 32 P-labelled double-stranded oligonucleotides encoding the EGR-1-binding element in the PNMT promoter (5 -CCTCCCGCCCCCGCGCGTCC-3 ) as a probe as described previously [33]. Protein-DNA complexes after separation on 5 % polyacrylamide gels were visualized by autoradiography.…”

Section: Author Contributionmentioning

confidence: 99%

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Heparanase enhances nerve-growth-factor-induced PC12 cell neuritogenesis via the p38 MAPK pathway

Cui

Shao

Liu

et al. 2011

Biochemical Journal

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Heparanase is involved in the cleavage of the HS (heparan sulfate) chain of HSPGs (HS proteoglycans) and hence participates in remodelling of the ECM (extracellular matrix) and BM (basement membrane). In the present study we have shown that NGF (nerve growth factor) promoted nuclear enrichment of EGR1 (early growth response 1), a transcription factor for heparanase, and markedly induced heparanase expression in rat adrenal pheochromocytoma (PC12) cells. K252a, an antagonist of the NGF receptor TrkA (tyrosine kinase receptor A), decreased heparanase protein expression induced by NGF in PC12 cells. Suramin, a heparanase inhibitor, decreased heparanase in PC12 cells and blocked NGF-induced PC12 neuritogenesis. Stable overexpression of heparanase activated p38 MAPK (mitogen-activated protein kinase) by phosphorylation and enhanced the neurite outgrowth induced by NGF, whereas knock down of heparanase impaired this process. However, overexpression of latent pro-heparanase with a Y156A mutation still led to enhanced NGF-induced neurite outgrowth and increased p38 MAPK phosphorylation. Inhibition of p38 MAPK by SB203580 suppressed the promotion of NGF-induced neuritogenesis by the wild-type and mutant heparanase. The impaired differentiation by knock down of heparanase could be restored by transfection of wild-type or mutant heparanase in PC12 cells. The results of the present study suggest that heparanase, at least in the non-enzymatic form, may promote NGF-induced neuritogenesis via the p38 MAPK pathway.

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Section: Ngf-induced Heparanase Expression In Pc12 Cells Is Attenuatesupporting

confidence: 93%

Section: Author Contributionmentioning

confidence: 99%

Heparanase enhances nerve-growth-factor-induced PC12 cell neuritogenesis via the p38 MAPK pathway

Cui

Shao

Liu

et al. 2011

Biochemical Journal

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“…In studies using PC12 cells that are widely used for examining NGF, others have shown that NGF increases the expression of certain genes by augmenting DNA binding or activity of transcription factors such as Sp1, c-fos, c-jun, Egr-1, and STAT3 etc. (Pierchala et al, 2004;Sobue et al, 2005;Ng et al, 2006;Pelligrino and Stork, 2006;Rojo et al, 2006;Tai et al, 2006). NGF signal is transduced through various pathways to activate transcription factors.…”

Section: Discussionmentioning

confidence: 99%

Epigenetic regulation of kappa opioid receptor gene in neuronal differentiation

Park

et al. 2008

Neuroscience

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The gene of mouse kappa opioid receptor (KOR) utilizes two promoters, P1 and P2. P1 is active in various brain areas and constitutively in P19 mouse embryonal carcinoma cells. P2 is active in limited brain stem areas of adult animals and only in late differentiated cells of P19 induced for neuronal differentiation in the presence of nerve growth factor (NGF). NGF response of P2 was found to be mediated by a specific binding site for transcription factor activation protein 2 (AP2) located in P2. Electrophoretic gel shift assay showed specific binding of this AP2 site by AP2beta, but not AP2alpha. Knockdown of endogenous AP2beta with siRNA abolished the stimulating effect of NGF on the expression of transcripts driven by P2. Binding of endogenous AP2beta on the endogenous KOR P2 chromatin region was also confirmed by chromatin immunoprecipitation. The effect of NGF was inhibited by LY2942002 (phosphatidylinositol 3-kinase, PI3K inhibitor), suggesting that PI3K was involved in signaling pathway mediating the effect of NGF stimulation on KOR P2. The chromatin of P2 in P19 was found to be specifically modified following NGF stimulation, which included demethylation at Lys9 and dimethylation at Lys4 of histone H3 and was consistent with the increased recruitment of RNA polymerase II to this promoter. This study presents the first evidence for epigenetic changes occurred on a specific KOR promoter triggered by NGF in cells undergoing neuronal differentiation. This epigenetic change is mediated by recruited AP2beta to this promoter and involves the PI3K system.

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“…The inflammatory cells or exposed nerves produce and release NGF, and the elevated circulating NGF regulates the conversion of chromaffin cells to neurons through upregulating p-ERK-JMJD3-Mash1 signaling and regulating peripherin and adrenergic expression via posttranscriptional control of the PNMT gene (29). The neuronal transition may provoke alternations in the morphology and function of AMCC, which reduce the baseline and stress-induced EPI levels and subsequently cause the ineffective dilatation of the bronchi.…”

Section: L608 Adrenal Medulla Cells Conversion In Eibmentioning

confidence: 99%

High-intensity training induces EIB in rats through neuron transdifferentiation of adrenal medulla chromaffin cells

Feng

Xun

et al. 2013

American Journal of Physiology-Lung Cellular and Molecular Phys

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He R, Feng J, Xun Q, Qin Q, Hu C. High-intensity training induces EIB in rats through neuron transdifferentiation of adrenal medulla chromaffin cells. Am J Physiol Lung Cell Mol Physiol 304: L602-L612, 2013. First published February 15, 2013 doi:10.1152/ajplung.00406.2012.-A high prevalence of exercise-induced bronchoconstriction (EIB) can be found in elite athletes, but the underlying mechanisms remain elusive. Airway responsiveness, NGF and epinephrine (EPI) levels, and chromaffin cell structure in high-(HiTr) and moderate-intensity training (MoTr) rats with or without ovalbumin (OVA) sensitization were measured in a total of 120 male Sprague-Dawley rats. The expression of NGF-associated genes in rat adrenal medulla was tested. Both HiTr and OVA intervention significantly increased airway resistance to aerosolized methacholine measured by whole body plethysmography. HiTr significantly increased inflammatory reaction in the lung with a major increase in peribronchial lymphocyte infiltration, whereas OVA significantly increased the infiltration of various inflammatory cells with an over 10-fold increase in eosinophil level in bronchoalveolar lavage. Both HiTr and OVA intervention upregulated circulating NGF level and peripherin level in adrenal medulla, but downregulated phenylethanolamine N-methyl transferase level in adrenal medulla and circulating EPI level. HiTr ϩ OVA and HiTr ϩ ExhEx (exhaustive exercise) interventions significantly enhanced most of the HiTr effects. The elevated NGF level was significantly associated with neuronal conversion of adrenal medulla chromaffin cells (AMCC). The levels of p-Erk1/2, JMJD3, and Mash1 were significantly increased, but the levels of p-p38 and p-JNK were significantly decreased in adrenal medulla in HiTr and OVA rats. Injection of NGF antiserum and moderate-intensity training reversed these changes observed in HiTr and/or OVA rats. Our study suggests that NGF may play a vital role in the pathogenesis of EIB by inducing neuron transdifferentiation of AMCC via MAPK pathways and subsequently decreasing circulating EPI. exercise; asthma; lung; inflammation; NGF; neuron conversion; adrenal medulla EXERCISE-INDUCED BRONCHOCONSTRICTION (EIB) is the increase in airway obstruction with symptoms of coughing, wheezing, or dyspnea as a result of exercise (23). EIB occurs in ϳ11% of the general population without asthma (13). Inhalation of cold air and sudden changes in humidity or temperature have been associated with EIB (20). High prevalence of EIB is usually observed among endurance athletes (7), implicating that intensity of exercise may be associated with EIB.Although thermal and osmotic consequences of water loss play prominent roles in the emergence of EIB (2), more studies are needed to elucidate the underlying mechanism. Circulating epinephrine (EPI), produced by adrenal medulla chromaffin cells (AMCC), is believed to bind the adrenergic receptors of airway smooth muscles to achieve adrenergic bronchodilation, and a loss of this function could directly influence the sev...

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Nerve Growth Factor Regulates Adrenergic Expression

Cited by 8 publications

References 57 publications

Heparanase enhances nerve-growth-factor-induced PC12 cell neuritogenesis via the p38 MAPK pathway

Heparanase enhances nerve-growth-factor-induced PC12 cell neuritogenesis via the p38 MAPK pathway

Epigenetic regulation of kappa opioid receptor gene in neuronal differentiation

High-intensity training induces EIB in rats through neuron transdifferentiation of adrenal medulla chromaffin cells

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