ArticleJournal of neurochemistry2015
Ethanol activates midkine and anaplastic lymphoma kinase signaling in neuroblastoma cells and in the brain.
Article in Journal of neurochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Implication of the PTN/RPTPβ/ζ Signaling Pathway in Acute Ethanol Neuroinflammation in Both Sexes: A Comparative Study with LPS.Biomedicines · 2023Article
- Binge-like ethanol drinking activates anaplastic lymphoma kinase signaling and increases the expression of STAT3 target genes in the mouse hippocampus and prefrontal cortex.Genes, brain, and behavior · 2021Article
- Binge-Like Ethanol Drinking IncreasesNeuroscience insights · 2021Article
- Anaplastic Lymphoma Kinase Regulates Internalization of the Dopamine D2 Receptor.Molecular pharmacology · 2020Article
- Receptor Tyrosine Kinases as Therapeutic Targets for Alcohol Use Disorder.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Review
- Connecting Metainflammation and Neuroinflammation Through the PTN-MK-RPTPβ/ζ Axis: Relevance in Therapeutic Development.Frontiers in pharmacology · 2019Review
- Pharmacological inhibition of Receptor Protein Tyrosine Phosphatase β/ζ (PTPRZ1) modulates behavioral responses to ethanol.Neuropharmacology · 2018Article
- Development of inhibitors of receptor protein tyrosine phosphatase β/ζ (PTPRZ1) as candidates for CNS disorders.European journal of medicinal chemistry · 2018Article
- Midkine in the mouse ventral tegmental area limits ethanol intake and Ccl2 gene expression.Genes, brain, and behavior · 2017Article
- From top to bottom: midkine and pleiotrophin as emerging players in immune regulation.Journal of leukocyte biology · 2017Review
- Anaplastic lymphoma kinase regulates binge-like drinking and dopamine receptor sensitivity in the ventral tegmental area.Addiction biology · 2017Article
- Anaplastic Lymphoma Kinase Is a Regulator of Alcohol Consumption and Excitatory Synaptic Plasticity in the Nucleus Accumbens Shell.Frontiers in pharmacology · 2017Article
- Mystic Acetaldehyde: The Never-Ending Story on Alcoholism.Frontiers in behavioral neuroscience · 2017Review
- Dependence-induced ethanol drinking and GABA neurotransmission are altered in Alk deficient mice.Neuropharmacology · 2016Article
- Using In Vitro Electrophysiology to Screen Medications: Accumbal Plasticity as an Engram of Alcohol Dependence.International review of neurobiology · 2016Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Alcohol engages signaling pathways in the brain. Midkine (MDK) is a neurotrophic factor that is over-expressed in the prefrontal cortex of alcoholics. MDK and one of its receptors, anaplastic lymphoma kinase (ALK), also regulate behavioral responses to ethanol in mice. The goal of this study was to determine whether MDK and ALK expression and signaling are activated by ethanol. We found that ethanol treatment of neuroblastoma cells increased MDK and ALK expression. We also assessed activation of ALK by ethanol in cells and found that ALK and ALK-dependent extracellular signal-regulated kinase (ERK) and signal transducer and activator of transcription 3 (STAT3) phosphorylation increased rapidly with ethanol exposure. Similarly, treatment of cells with recombinant MDK protein increased ALK, ERK and STAT3 phosphorylation, suggesting that ethanol may utilize MDK to activate ALK signaling. In support of this, transfection of cells with MDK siRNAs attenuated ALK signaling in response to ethanol. Ethanol also activates ERK signaling in the brain. We found that inhibition of ALK or knockout of MDK attenuated ethanol-induced ERK phosphorylation in mouse amygdala. These results demonstrate that ethanol engages MDK and ALK signaling, which has important consequences for alcohol-induced neurotoxicity and the regulation of behaviors related to alcohol abuse.
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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.