ArticleHepatology (Baltimore, Md.)2009
Adenosine induces loss of actin stress fibers and inhibits contraction in hepatic stellate cells via Rho inhibition.
Article in Hepatology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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Who cites it
38 citing papers in PubMed, 90 citations in OpenAlex.
- Purinergic signaling and cholangiocyte regeneration: a new frontier in ischemic liver injury.Frontiers in transplantation · 2025Review
- Purinergic Signaling in Non-Parenchymal Liver Cells.International journal of molecular sciences · 2024Review
- Orphan receptor GPR176 in hepatic stellate cells exerts a profibrotic role in chronic liver disease.JHEP reports : innovation in hepatology · 2024Article
- Survivin inhibition ameliorates liver fibrosis by inducing hepatic stellate cell senescence and depleting hepatic macrophage population.Journal of cell communication and signaling · 2024Article
- Coffee, adenosine, and the liver.Purinergic signalling · 2024Review
- Interaction of non‑parenchymal hepatocytes in the process of hepatic fibrosis (Review).Molecular medicine reports · 2021Review
- Resveratrol increases the activation markers and changes the release of inflammatory cytokines of hepatic stellate cells.Molecular and cellular biochemistry · 2021Article
- Restraint of Human Skin Fibroblast Motility, Migration, and Cell Surface Actin Dynamics, by Pannexin 1 and P2X7 Receptor Signaling.International journal of molecular sciences · 2021Article
- Role of G Protein-Coupled Receptors in Hepatic Stellate Cells and Approaches to Anti-Fibrotic Treatment of Non-Alcoholic Fatty Liver Disease.Frontiers in endocrinology · 2021Review
- Purinergic signalling in liver diseases: Pathological functions and therapeutic opportunities.JHEP reports : innovation in hepatology · 2020Review
- Levistilide A reverses rat hepatic fibrosis by suppressing angiotensin II‑induced hepatic stellate cells activation.Molecular medicine reports · 2020Article
- Reduction in SNAP-23 Alters Microfilament Organization in Myofibrobastic Hepatic Stellate Cells.Gene expression · 2020Article
- A High-Throughput Workflow to Study Remodeling of Extracellular Matrix-Based Microtissues.Tissue engineering. Part C, Methods · 2019Article
- Thrombin and factor Xa link the coagulation system with liver fibrosis.BMC gastroenterology · 2018Article
- Hepatic stellate cells as key target in liver fibrosis.Advanced drug delivery reviews · 2017Review
- Adenosine receptor signaling: a key to opening the blood-brain door.Fluids and barriers of the CNS · 2015Review
- A2A Adenosine Receptor Regulates the Human Blood-Brain Barrier Permeability.Molecular neurobiology · 2015Article
- Hepatic arterial vasodilation is independent of portal hypertension in early stages of cirrhosis.PloS one · 2015Article
- I drink for my liver, Doc: emerging evidence that coffee prevents cirrhosis.F1000Research · 2015Review
- Sodium ferulate lowers portal pressure in rats with secondary biliary cirrhosis through the RhoA/Rho-kinase signaling pathway: a preliminary study.International journal of molecular medicine · 2014Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The Rho/ROCK pathway is activated in differentiated hepatic stellate cells (HSCs) and is necessary for assembly of actin stress fibers, contractility, and chemotaxis. Despite the importance of this pathway in HSC biology, physiological inhibitors of the Rho/ROCK pathway in HSCs are not known. We demonstrate that adenosine induces loss of actin stress fibers in the LX-2 cell line and primary HSCs in a manner indistinguishable from Rho/ROCK inhibition. Loss of actin stress fibers occurs via the A2a receptor at adenosine concentrations above 10 muM, which are present during tissue injury. We further demonstrate that loss of actin stress fibers is due to a cyclic adenosine monophosphate, protein kinase A-mediated pathway that results in Rho inhibition. Furthermore, a constitutively active Rho construct can inhibit the ability of adenosine to induce loss of actin stress fibers. Actin stress fibers are required for HSC contraction, and we demonstrate that adenosine inhibits endothelin-1 and lysophosphatidic acid-mediated HSC contraction. We propose that adenosine is a physiological inhibitor of the Rho pathway in HSCs with functional consequences, including loss of HSC contraction.
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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.