ArticleJournal of vascular research2015
G-Protein-Coupled Receptor 35 Mediates Human Saphenous Vein Vascular Smooth Muscle Cell Migration and Endothelial Cell Proliferation.
Article in Journal of vascular research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
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
16 citing papers in PubMed, 28 citations in OpenAlex.
- GPR35 Mediates the Proliferation and Adipogenesis of Goat Intramuscular Preadipocytes Through the cAMP/PKA Signaling Pathway.Animals : an open access journal from MDPI · 2026Article
- G Protein-Coupled Receptor 35 Suppresses Oxidative Stress Responsive Kinase 1 in Diabetic Wound Healing.Diabetes · 2025Article
- The power of many: Multilevel targeting of representative chemokine and metabolite GPCRs in personalized cancer therapy.European journal of immunology · 2024Review
- Spatial multi-omics characterizes GPR35-relevant lipid metabolism signatures across liver zonation in MASLD.Life metabolism · 2024Article
- From orphan to oncogene: The role of GPR35 in cancer and immune modulation.Cytokine & growth factor reviews · 2024Review
- GPR35 and mediators from platelets and mast cells in neutrophil migration and inflammation.Immunological reviews · 2023Review
- Recent advances in GPR35 pharmacology; 5-HIAA serotonin metabolite becomes a ligand.Archives of pharmacal research · 2023Review
- GPR35 antagonist CID-2745687 attenuates anchorage-independent cell growth by inhibiting YAP/TAZ activity in colorectal cancer cells.Frontiers in pharmacology · 2023Article
- G Protein-Coupled Receptor GPR35 Suppresses Lipid Accumulation in Hepatocytes.ACS pharmacology & translational science · 2021Article
- G-protein coupled receptor 35 (GPR35) regulates the colonic epithelial cell response to enterotoxigenic Bacteroides fragilis.Communications biology · 2021Article
- Therapeutic Opportunities and Challenges in Targeting the Orphan G Protein-Coupled Receptor GPR35.ACS pharmacology & translational science · 2020Review
- Adopting an Orphan: How Could GRP35 Contribute to Angiotensin II-Dependent Hypertension?American journal of hypertension · 2018Article
- The Orphan Receptor GPR35 Contributes to Angiotensin II-Induced Hypertension and Cardiac Dysfunction in Mice.American journal of hypertension · 2018Article
- G protein-coupled receptors not currently in the spotlight: free fatty acid receptor 2 and GPR35.British journal of pharmacology · 2018Review
- Inhibition of miR-155 attenuates abdominal aortic aneurysm in mice by regulating macrophage-mediated inflammation.Bioscience reports · 2018Article
- Overexpression of GPR35 confers drug resistance in NSCLC cells by β-arrestin/Akt signaling.OncoTargets and therapy · 2018Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Vascular smooth muscle cell (VSMC) migration and proliferation is central to neointima formation in vein graft failure following coronary artery bypass. However, there are currently no pharmacological interventions that prevent vein graft failure through intimal occlusion. It is hence a therapeutic target. Here, we investigated the contribution of GPR35 to human VSMC and endothelial cell (EC) migration, using a scratch-wound assay, and also the contribution to proliferation, using MTS and BrdU assays, in in vitro models using recently characterized human GPR35 ortholog-selective small-molecule agonists and antagonists. Real-time PCR studies showed GPR35 to be robustly expressed in human VSMCs and ECs. Stimulation of GPR35, with either the human-selective agonist pamoic acid or the reference agonist zaprinast, promoted VSMC migration in the scratch-wound assay. These effects were blocked by coincubation with either of the human GPR35-specific antagonists, CID-2745687 or ML-145. These GPR35-mediated effects were produced by inducing alterations in the actin cytoskeleton via the Rho A/Rho kinase signaling axis. Additionally, the agonist ligands stimulated a proliferative response in ECs. These studies highlight the potential that small molecules that stimulate or block GPR35 activity can modulate vascular proliferation and migration. These data propose GPR35 as a translational therapeutic target in vascular remodeling.
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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.