ArticleJournal of neurochemistry2012
gp130 cytokines stimulate proteasomal degradation of tyrosine hydroxylase via extracellular signal regulated kinases 1 and 2.
Article in Journal of neurochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Autonomic nervous system and cardiac neuro-signaling pathway modulation in cardiovascular disorders and Alzheimer's disease.Frontiers in physiology · 2023Review
- Trojan Horse Delivery of 4,4'-Dimethoxychalcone for Parkinsonian Neuroprotection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Proteasome-mediated degradation of tyrosine hydroxylase triggered by its phosphorylation: a new question as to the intracellular location at which the degradation occurs.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- ERK5 induces ankrd1 for catecholamine biosynthesis and homeostasis in adrenal medullary cells.Cellular signalling · 2016Article
- Myocardial Infarction Causes Transient Cholinergic Transdifferentiation of Cardiac Sympathetic Nerves via gp130.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Trace Amine-Associated Receptor 1 Regulation of Methamphetamine Intake and Related Traits.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015Article
- Cardiac innervation and sudden cardiac death.Circulation research · 2015Review
- Targeting protein tyrosine phosphatase σ after myocardial infarction restores cardiac sympathetic innervation and prevents arrhythmias.Nature communications · 2015Article
- Complex molecular regulation of tyrosine hydroxylase.Journal of neural transmission (Vienna, Austria : 1996) · 2014Review
- Sympathetic denervation of peri-infarct myocardium requires the p75 neurotrophin receptor.Experimental neurology · 2013Article
- STAT3 integrates cytokine and neurotrophin signals to promote sympathetic axon regeneration.Molecular and cellular neurosciences · 2013Article
- LIF and the heart: just another brick in the wall?European cytokine network · 2013Review
- A possible pathophysiological role of tyrosine hydroxylase in Parkinson's disease suggested by postmortem brain biochemistry: a contribution for the special 70th birthday symposium in honor of Prof. Peter Riederer.Journal of neural transmission (Vienna, Austria : 1996) · 2013Review
- Ciliary neurotrophic factor stimulates tyrosine hydroxylase activity.Journal of neurochemistry · 2012Article
- gp130 cytokines are positive signals triggering changes in gene expression and axon outgrowth in peripheral neurons following injury.Frontiers in molecular neuroscience · 2011Article
- Infarction-induced cytokines cause local depletion of tyrosine hydroxylase in cardiac sympathetic nerves.Experimental physiology · 2010Article
- Review
Corrections and comments
- Commented on by
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Injury-induced cytokines act through gp130 in sympathetic neurons to suppress expression of tyrosine hydroxylase (TH) and other genes associated with noradrenergic transmission. These cytokines also trigger the local loss of TH in peri-infarct sympathetic axons after myocardial infarction, but altered gene expression cannot explain the selective loss of TH enzyme in one region of the heart. We hypothesized that inflammatory cytokines, which are highest near the infarct, stimulated local degradation of TH protein. We used cultured sympathetic neurons and neuroblastoma cells to test this hypothesis. The cytokines ciliary neurotrophic factor (CNTF) and leukemia inhibitory factor (LIF) suppressed TH content in both neurons and neuroblastoma cells. CNTF suppressed TH in a gp130-dependent manner, and decreased the half-life of TH protein by approximately 50%. CNTF stimulated the ubiquitination of TH in both neurons and neuroblastoma cells, and the proteasome inhibitors MG-132 and lactacystin prevented the CNTF-induced loss of TH protein. Inhibiting activation of extracellular signal regulated kinases 1&2 (ERK1/2) with U0126 prevented the CNTF-induced ubiquitination of TH and the associated decrease in protein half-life. Likewise, inhibiting ERK1/2 activation blunted the cytokine-stimulated loss of TH protein in sympathetic neurons, despite enhancing the loss of TH mRNA. These data suggest that gp130 cytokines stimulate proteasomal degradation of TH through an ERK1/2 dependent pathway, and may have important implications for local regulation of neurotransmission at sites of inflammation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.