ArticleBritish journal of pharmacology2010
Thrombospondin-1 is an inhibitor of pharmacological activation of soluble guanylate cyclase.
Article in British journal of pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 56 citations in OpenAlex.
- Per-ARNT-Sim Domains in Nitric Oxide Signaling by Soluble Guanylyl Cyclase.Journal of molecular biology · 2024Review
- The NO/cGMP/PKG pathway in platelets: The therapeutic potential of PDE5 inhibitors in platelet disorders.Journal of thrombosis and haemostasis : JTH · 2022Review
- Indirect mediators of systemic health outcomes following nanoparticle inhalation exposure.Pharmacology & therapeutics · 2022Review
- Efficient Ex Vivo Screening of Agents Targeting Thrombospondin1-Induced Vascular Dysfunction Using a Digital Multiwire Myograph System.Methods and protocols · 2021Article
- A Potential Role of the CD47/SIRPalpha Axis in COVID-19 Pathogenesis.Current issues in molecular biology · 2021Article
- Novel Pharmaceutical Strategy for Selective Abrogation of TSP1-Induced Vascular Dysfunction by Decoy Recombinant CD47 Soluble Receptor in Prophylaxis and Treatment Models.Biomedicines · 2021Article
- Thrombospondin-1 CD47 Signalling: From Mechanisms to Medicine.International journal of molecular sciences · 2021Review
- Extracellular matrix dynamics in vascular remodeling.American journal of physiology. Cell physiology · 2020Review
- Mathematical Model Predicts Effective Strategies to Inhibit VEGF-eNOS Signaling.Journal of clinical medicine · 2020Article
- Regulation of Cellular Redox Signaling by Matricellular Proteins in Vascular Biology, Immunology, and Cancer.Antioxidants & redox signaling · 2017Article
- Thrombospondin-1, Free Radicals, and the Coronary Microcirculation: The Aging Conundrum.Antioxidants & redox signaling · 2017Review
- Matricellular protein thrombospondin-1 in pulmonary hypertension: multiple pathways to disease.Cardiovascular research · 2017Review
- Nitric oxide: what's new to NO?American journal of physiology. Cell physiology · 2017Review
- Thrombospondin-1 mediates multi-walled carbon nanotube induced impairment of arteriolar dilation.Nanotoxicology · 2017Article
- The role of circulating thrombospondin-1 in patients with precapillary pulmonary hypertension.Respiratory research · 2016Observational
- Physiological levels of thrombospondin-1 decrease NO-dependent vasodilation in coronary microvessels from aged rats.American journal of physiology. Heart and circulatory physiology · 2016Article
- Article
- Thrombospondin-1-Based Antiangiogenic Therapy.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2015Article
- CD47 signaling pathways controlling cellular differentiation and responses to stress.Critical reviews in biochemistry and molecular biology · 2015Review
- Aging of the nitric oxide system: are we as old as our NO?Journal of the American Heart Association · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
background and purposeSoluble guanylate cyclase (sGC) is the signal transduction enzyme most responsible for mediating the effects of nitric oxide (NO). Recently, NO-independent small molecule activators of sGC have been developed that have promising clinical activities. We have shown that the secreted matrix protein thrombospondin-1 (TSP-1) binds to CD47 and potently inhibits NO stimulation of sGC in endothelial and vascular smooth muscle cells (VSMCs) and platelets. Here we show that TSP-1 signalling via CD47 inhibits sGC activation by NO-independent sGC activating small molecules. EXPERIMENTAL APPROACH: Vascular smooth muscle cells and washed human platelets were pretreated with TSP-1 (2.2 nM) in the presence of haeme-dependent sGC activators (YC-1, BAY 41-2272), and a haeme-independent activator (meso-porphyrin IX), and cGMP levels were measured. The effect of sGC activators on platelet aggregation and contraction of VSMC embedded in collagen gels was also assayed in the presence and absence of TSP-1. KEY
resultsThrombospondin-1 inhibited sGC activator-dependent increase in cGMP in VSMC and platelets. TSP-1 pretreatment also inhibited the ability of these agents to delay thrombin-induced platelet aggregation. TSP-1 pretreatment reduced the ability of sGC activating agents to abrogate VSMC contraction in vitro. CONCLUSIONS AND IMPLICATIONS: This work demonstrates that TSP-1 is a universal inhibitor of sGC, blocking both haeme-dependent and haeme-independent activation. These data coupled with the reported increases in TSP-1 with age, diabetes, ischaemia/reperfusion, and atherosclerosis implies that the therapeutic potential of all drugs that activate sGC could be compromised in disease states where TSP-1/CD47 signalling is elevated.
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.