Activated Transcription of the Human Neuropeptide Y Gene in Differentiating SH‐SY5Y Neuroblastoma Cells Is Dependent on Transcription Factors AP‐1, AP‐2α, and NGFI

Wernersson, Jonny; Johansson, Iva; Larsson, Ulrika; Minth-Worby, Carolyn; Påhlman, Sven; Andersson, Gerhard

doi:10.1046/j.1471-4159.1998.70051887.x

Cited by 36 publications

(21 citation statements)

References 23 publications

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“…NGFI-A transcription factor has also been shown to be involved in activating NPY transcription during the onset of neuronal differentiation. 35 Thus, our data support the hypothesis that upregulation of NGFI-A with activation of several downstream signal pathways may be involved in promoting scarless healing (Fig. 1).…”

Section: Discussionsupporting

confidence: 87%

Upregulation of Neurodevelopmental Genes During Scarless Healing

Antony¹,

Kong²,

Lorenz³

2010

Annals of Plastic Surgery

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Scarless fetal skin wound healing is a paradigm for ideal skin repair and is dependent on peripheral nerve function.To further explore neurogenic mechanisms influence on the scarless skin repair, fetal rats were wounded on gestational days 16 (E16; n = 24) and 18 (E18; n = 8) and wounds were harvested at 1 and 3 days after injury. Unwounded skin at identical gestational age was used for control comparison. The scarless E16 and scarring E18 wounds underwent macroarray gene expression analysis (1172 genes).During the scarless healing period, 53 (4.5%) genes had a statistically significant upregulation post-injury with at least a 2- to 3-fold change 1 day after wounding and 14 (1.2%) genes 3 days after wounding (P < 0.05). Many neurodevelopmental genes were increased during scarless repair on post-injury days 1 and 3. Neuropeptide Y Receptor type I, cJun related Transcription Factor (junD), Synaptophysin, SNAP 25, Neuronal calcium sensor 1 (NCS1), neural visine-like calcium binding protein 1 (NVP1), nerve growth factor-induced gene A (NGFI-A/EGR1), VGF8A protein, p27kip1, and members of the GABA and serotonin family each had 2- to 3-fold expression increases (P < 0.05).We speculate that fetal skin cells express neurotrophins during skin development that regulate peripheral neuron formation. During injury these factors promote the survival and regeneration of peripheral neurons; this interaction of neuropeptides, neuropeptide receptors, and neurotrophins may modulate the fetal scarless repair mechanisms in response to injury. Identification of these neurodevelopmental candidate genes provides insight for new investigation into mechanisms regulating scarless healing.

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Section: Discussionsupporting

confidence: 87%

Upregulation of Neurodevelopmental Genes During Scarless Healing

Antony¹,

Kong²,

Lorenz³

2010

Annals of Plastic Surgery

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“…On the molecular level, this selective NPY regulation could be due to transcription factors acting directly on the NPY promoter such as NGFI-A, AP-1, AP-2, and retinoic acid, which might act with different potencies on the promoter of the NPY gene in the two strains (Buckland et al, 2004;Jalava and Mai, 1994;Li et al, 2000;Magni et al, 2000;Wernersson et al, 1998). Moreover, it is conceivable that there is a set of factors controlling basal transcription and another set that is induced after running.…”

Section: Discussionmentioning

confidence: 99%

Running has Differential Effects on NPY, Opiates, and Cell Proliferation in an Animal Model of Depression and Controls

Bjørnebekk

Mathé

Brené

2005

Neuropsychopharmacol

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Physical activity has documented beneficial effect in treatment of depression. Recently, we found an antidepressant-like effect of running in an animal model of depression, the Flinders Sensitive Line (FSL) and demonstrated that it was associated with increased hippocampal cell proliferation. In this study, we analyzed levels of mRNAs encoding the neuropeptide Y (NPY) and the opioid peptides dynorphin and enkephalin in hippocampus and correlated these to cell proliferation in the FSL and in the 'nondepressed' Flinders Resistant Line (FRL) strain, with/without access to running wheels. Running increased NPY mRNA in dentate gyrus and the CA4 region in FSL, but not in FRL rats. NPY mRNA increase was correlated to increased cell proliferation in the subgranular zone of dentate gyrus. Baseline dynorphin and enkephalin mRNA levels in the dentate gyrus were lower in the FSL compared to the FRL strain. Running had no effect on dynorphin and enkephalin mRNAs in the FSL strain but it decreased dynorphin mRNA, and there was a trend to increased enkephalin mRNA in the FRL rats. Thus, it would appear that the CNS effects of running are different in 'depressed' and control animals; modification of NPY, a peptide associated with depression and anxiety, in depressed animals, vs effects on opioids, associated with the reward systems, in healthy controls. Our data support the hypothesis that NPY neurotransmission in hippocampus is malfunctioning in depression and that antidepressive treatment, in this case wheel running, will normalize it. In addition, we also show that the increased NPY after running is correlated to increased cell proliferation, which is associated with an antidepressive-like effect.

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“…The increase in protein production is consistent with the abundant rough endoplasmic reticulum found in the cells. Pro-enkephalin and NPY gene expression are controlled by AP1 transcription factor, which may mediate this increase (39,40).…”

Section: Discussionmentioning

confidence: 99%

Deletion of tyrosine hydroxylase gene reveals functional interdependence of adrenocortical and chromaffin cell system in vivo

Bornstein

Tian

Haidan

et al. 2000

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

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Catecholamines are produced in the medulla of the adrenal gland and may participate in the intraglandular regulation of its cortex. We analyzed the adrenal structure and function of albino tyrosine hydroxylase-null (TH-null) mice that are deficient in adrenal catecholamine production. Adrenal catecholamines were markedly reduced, and catecholamine histofluorescence was abrogated in 15-day-old TH-null mice. Chromaffin cell structure was strikingly altered at the ultrastructural level with a depletion of chromaffin vesicles and an increase in rough endoplasmic reticulum compared with wild-type mice. Remaining chromaffin vesicles lined up proximally to the cell membrane in preparation for exocytosis providing a ''string-ofpearls'' appearance. There was a 5-fold increase in the expression of proenkephalin mRNA (502.8 ؎ 142% vs. 100 ؎ 17.5%, P ‫؍‬ 0.016) and a 2-fold increase in the expression of neuropeptide Y (213.4 ؎ 41.2% vs. 100 ؎ 59.9%, P ‫؍‬ 0.014) in the TH-null animals as determined by quantitative TaqMan (Perkin-Elmer) PCR. Accordingly, immunofluorescence for met-enkephalin and neuropeptide tyrosine in these animals was strongly enhanced. The expression of phenylethanolamine N-methyl transferase and chromogranin B mRNA was similar in TH-null and wild-type mice. In TH-null mice, adrenocortical cells were characterized by an increase in liposomes and by tubular mitochondria with reduced internal membranes, suggesting a hypofunctional state of these steroid-producing cells. In accordance with these findings, plasma corticosterone levels were decreased. Plasma ACTH levels were not significantly different in TH-null mice. In conclusion, both the adrenomedullary and adrenocortical systems demonstrate structural and functional changes in catecholaminedeficient TH-null mice, underscoring the great importance of the functional interdependence of these systems in vivo.

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Activated Transcription of the Human Neuropeptide Y Gene in Differentiating SH‐SY5Y Neuroblastoma Cells Is Dependent on Transcription Factors AP‐1, AP‐2α, and NGFI

Cited by 36 publications

References 23 publications

Upregulation of Neurodevelopmental Genes During Scarless Healing

Upregulation of Neurodevelopmental Genes During Scarless Healing

Running has Differential Effects on NPY, Opiates, and Cell Proliferation in an Animal Model of Depression and Controls

Deletion of tyrosine hydroxylase gene reveals functional interdependence of adrenocortical and chromaffin cell system in vivo

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