ArticlePloS one2012
Extracellular nucleotides inhibit insulin receptor signaling, stimulate autophagy and control lipoprotein secretion.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- The dual roles of autophagy and the GPCRs-mediating autophagy signaling pathway after cerebral ischemic stroke.Molecular brain · 2022Review
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- The Adenosine Pathway and Human Immunodeficiency Virus-Associated Inflammation.Open forum infectious diseases · 2021Review
- Clodronate, an inhibitor of the vesicular nucleotide transporter, ameliorates steatohepatitis and acute liver injury.Scientific reports · 2021Article
- Purinergic signalling in liver diseases: Pathological functions and therapeutic opportunities.JHEP reports : innovation in hepatology · 2020Review
- P2YGlia · 2020Article
- Extracellular ATP Increases Glucose Metabolism in Skeletal Muscle Cells in a P2 Receptor Dependent Manner but Does Not Contribute to Palmitate-Induced Insulin Resistance.Frontiers in physiology · 2020Article
- New Potential Pharmacological Functions of Chinese Herbal Medicines via Regulation of Autophagy.Molecules (Basel, Switzerland) · 2016Review
- Testosterone regulates the autophagic clearance of androgen binding protein in rat Sertoli cells.Scientific reports · 2015Article
- The PRKAA1/AMPKα1 pathway triggers autophagy during CSF1-induced human monocyte differentiation and is a potential target in CMML.Autophagy · 2015Article
- P2X receptors regulate adenosine diphosphate release from hepatic cells.Purinergic signalling · 2014Article
- Impairment of vesicular ATP release affects glucose metabolism and increases insulin sensitivity.Scientific reports · 2014Article
- G protein-coupled receptors and the regulation of autophagy.Trends in endocrinology and metabolism: TEM · 2014Review
- Purinergic signalling in the liver in health and disease.Purinergic signalling · 2014Review
- Purinergic signalling in endocrine organs.Purinergic signalling · 2014Review
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperglycemia is associated with abnormal plasma lipoprotein metabolism and with an elevation in circulating nucleotide levels. We evaluated how extracellular nucleotides may act to perturb hepatic lipoprotein secretion. Adenosine diphosphate (ADP) (>10 µM) acts like a proteasomal inhibitor to stimulate apoB100 secretion and inhibit apoA-I secretion from human liver cells at 4 h and 24 h. ADP blocks apoA-I secretion by stimulating autophagy. The nucleotide increases cellular levels of the autophagosome marker, LC3-II, and increases co-localization of LC3 with apoA-I in punctate autophagosomes. ADP affects autophagy and apoA-I secretion through P2Y(13). Overexpression of P2Y(13) increases cellular LC3-II levels by ~50% and blocks induction of apoA-I secretion. Conversely, a siRNA-induced reduction in P2Y(13) protein expression of 50% causes a similar reduction in cellular LC3-II levels and a 3-fold stimulation in apoA-I secretion. P2Y(13) gene silencing blocks the effects of ADP on autophagy and apoA-I secretion. A reduction in P2Y(13) expression suppresses ERK1/2 phosphorylation, increases the phosphorylation of IR-β and protein kinase B (Akt) >3-fold, and blocks the inhibition of Akt phosphorylation by TNFα and ADP. Conversely, increasing P2Y(13) expression significantly inhibits insulin-induced phosphorylation of insulin receptor (IR-β) and Akt, similar to that observed after treatment with ADP. Nucleotides therefore act through P2Y(13), ERK1/2 and insulin receptor signaling to stimulate autophagy and affect hepatic lipoprotein secretion.
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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.