c‐Fos is essential for the response of the tyrosine hydroxylase gene to depolarization or phorbol ester

Sun, Baoyong; Tank, A. William

doi:10.1046/j.1471-4159.2003.01789.x

Cited by 20 publications

(16 citation statements)

References 39 publications

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“…(1997) provide evidence that both the CRE and AP‐1 sites are involved and that c‐Fos, c‐Jun, JunB, and JunD are participant transcription factors in the inducible TH AP‐1 complex (Nagamoto‐Combs et al. 1997), supported also by (Sun and Tank 2003). However, Nankova et al.…”

Section: Ca2+‐sensitive Regulatory Elements In the Th Gene Promoter Amentioning

confidence: 96%

Activity‐dependent regulation of the dopamine phenotype in substantia nigra neurons

Aumann

Horne

2012

Journal of Neurochemistry

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The impetus behind this review is the question of whether the dopamine (DA) phenotype of neurons in the substantia nigra pars compacta (SNc) is activity-dependent. SNc DA neurons control movement through their projections to, and DA signaling in the dorsal striatum (the nigrostriatal pathway). Abnormal reduction of nigrostriatal DA signaling causes the motor symptoms of Parkinson's disease (PD), and abnormal DA signaling originating from the ventral midbrain generally (i.e. the nigrostriatal and mesocorticolimbic pathways) is thought to underlie symptoms of schizophrenia, drug addiction, and depression. The possibility that the DA phenotype of SNc neurons is activity-dependent is therefore intriguing from the viewpoints of neurobiology, behavior, and neurological disorders.Gene expression in neurons is activity-and Ca 2+ -dependent. More specifically, gene expression is sensitive to

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Section: Ca2+‐sensitive Regulatory Elements In the Th Gene Promoter Amentioning

confidence: 96%

Activity‐dependent regulation of the dopamine phenotype in substantia nigra neurons

Aumann

Horne

2012

Journal of Neurochemistry

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“…TH. At a molecular level, our proposed mechanism of G-CSF action in inducing MTA1 via c-Fos is supported by the findings that G-CSF triggers a de novo induction of c-Fos, and overexpression of c-Fos is sufficient to stimulate TH gene transcription (44,45). Furthermore, this induction of c-Fos by G-CSF was shown to be modulated by both MAPK and STAT3 signaling pathways (34,46).…”

Section: Discussionmentioning

confidence: 71%

Molecular Mechanism of Regulation of MTA1 Expression by Granulocyte Colony-stimulating Factor

Kumar

Jagadeeshan

Subramanian

et al. 2016

Journal of Biological Chemistry

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Parkinson disease (PD) is a neurodegenerative disorder with loss of dopaminergic neurons of the brain, which results in insufficient synthesis and action of dopamine. Metastasis-associated protein 1 (MTA1) is an upstream modulator of tyrosine hydroxylase (TH), the rate-limiting enzyme in dopamine synthesis, and hence MTA1 plays a significant role in PD pathogenesis. To impart functional and clinical significance to MTA1, we analyzed MTA1 and TH levels in the substantia nigra region of a large cohort of human brain tissue samples by Western blotting, quantitative PCR, and immunohistochemistry. Our results showed that MTA1 and TH levels were significantly down-regulated in PD samples as compared with normal brain tissue. Correspondingly, immunohistochemistry analysis for MTA1 in substantia nigra sections revealed that 74.1% of the samples had a staining intensity of <6 in the PD samples as compared with controls, 25.9%, with an odds ratio of 8.54. Because of the clinical importance of MTA1 established in PD, we looked at agents to modulate MTA1 expression in neuronal cells, and granulocyte colony-stimulating factor (G-CSF) was chosen, due to its clinically proven neurogenic effects. Treatment of the human neuronal cell line KELLY and acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model with G-CSF showed significant induction of MTA1 and TH with rescue of phenotype in the mouse model. Interestingly, the observed induction of TH was compromised on silencing of MTA1. The underlying molecular mechanism of MTA1 induction by G-CSF was proved to be through induction of c-Fos and its recruitment to the MTA1 promoter. Parkinson disease (PD)4 is an idiopathic degenerative disorder of the central nervous system characterized by slow and decreased movement, pill-rolling tremor, and postural instability, and it is primarily caused by dopamine deficiency (1, 2). The rate-limiting enzyme for dopamine synthesis is tyrosine hydroxylase (TH) (3). Currently, there is no cure for PD, and patients are usually given drugs that provide symptomatic relief (4). Recently, it was shown that G-CSF enhances recovery in the mouse model of PD, and hence the G-CSF receptor might be a novel target for modifying the disease process in PD (5, 6). It is well documented that a consistent abnormality in PD is degeneration of dopaminergic neurons in SN leading to a reduction of striatal dopamine levels (7). TH catalyzes the formation of L-hydroxyphenylalanine, the rate-limiting step in the biosynthesis of dopamine. Thus, efficient treatment strategy for PD could be based on correcting or bypassing the TH enzyme deficiency or its downstream enzymes essential for catecholamine synthesis (8). For this, elucidation of the molecular mechanism of human TH gene regulation is very essential. Also, epigenetic profiling of the human TH promoter suggests that chromatin remodeling could have a significant impact in conferring tissue-specific gene expression of the human TH gene (9); however, its specific role in TH transcription remains poorly understood...

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“…adrenergic receptor [37][38][39] . Acute intracerebroventricular (icv) injection of relaxin-3 induced an increase in Fos protein expression, a molecular marker of neuronal activation, in the hypothalamic regions such as the paraventricular hypothalamic nucleus (PVN), arcuate hypothalamic nucleus (ARC), supraoptic nucleus(SON), and lateral hypothalamus [40,41] .…”

Section: Relaxin Family Peptides and Elaxin Family Peptides And Its Rmentioning

confidence: 99%

The role of relaxin-3 and its receptor RXFP3 in defense of elevated body weight in diet-induced obesity

Lenglos

Calvez

Timofeeva

2014

Receptor Clin Invest

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Incidence of overweight and obesity has dramatically increased during the past three decades. Treatment of this serious clinical problem is hindered by the fact that once obesity has developed, the elevated body weight is defended against weight-decreasing treatment strategies by mechanisms that are not yet fully understood. This review focuses on the neuronal mechanisms that contribute to the maintenance of obesity after it development in the DIO rat model. Among the neuronal factors regulating energy intake, orexigenic neuropeptide relaxin-3 and its cognate receptor RXFP3 may play an important role in the defense of elevated body weight in DIO. The levels of expression of relaxin-3 mRNA in the brainstem nucleus incertus (NI) were significantly increased in thead libitum feeding state in DIO rats compared to DR rats. However, the effects of relaxin-3 in the DIO ad libitumfed rats may be compensated by a significant decrease in the levels of expression of RXFP3 mRNA in the food intake-regulating brain regions of DIO rats including the paraventricular hypothalamic nucleus (PVN), central amygdala (CeA), NI, and nucleus of the solitary tract (NTS). Remarkably, the DIO rats showed an immediate rebound in food intake at refeeding and regained all body weight lost during starvation. This significant increase in food intake during refeeding was accompanied by an increase in the levels of expression of RXFP3 in the parvocellular PVN, CeA, NI, and NTS in the DIO rats to the levels of the DR rats. Moreover, the expression of RXFP3 in the paraventricular thalamic nucleus was significantly higher in the refed DIO rats compared to the DR counterparts. A constitutive increase in the expression of relaxin-3 accompanied by a relative increase in the expression of RXFP3 in food intake-regulating brain regions during refeeding after food deprivation may contribute to the mechanisms of defense of elevated body weight in the DIO phenotype.

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c‐Fos is essential for the response of the tyrosine hydroxylase gene to depolarization or phorbol ester

Cited by 20 publications

References 39 publications

Activity‐dependent regulation of the dopamine phenotype in substantia nigra neurons

Activity‐dependent regulation of the dopamine phenotype in substantia nigra neurons

Molecular Mechanism of Regulation of MTA1 Expression by Granulocyte Colony-stimulating Factor

The role of relaxin-3 and its receptor RXFP3 in defense of elevated body weight in diet-induced obesity

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