ArticlePharmacological research2011
Thrombospondin-1 inhibition of vascular smooth muscle cell responses occurs via modulation of both cAMP and cGMP.
Article in Pharmacological research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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.
The trial behind it
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Who cites it
46 citing papers in PubMed, 73 citations in OpenAlex.
- Proteomics and human microchips identify Thrombospondin-1 as a potential biomarker for calciphylaxis stem cell therapy.iScience · 2026Article
- Thrombospondin 1-CD47 Signalling Modulates Vascular Smooth Muscle Cell Senescence in Chronic Kidney Disease.International journal of molecular sciences · 2026Article
- Article
- The mechanobiology of extracellular matrix: a focus on thrombospondins.Cell communication and signaling : CCS · 2025Review
- CD47-mediated tumor microenvironment remodeling: a central mechanism in immune evasion.Acta biochimica et biophysica Sinica · 2025Review
- Cell autonomous functions of CD47 in regulating cellular plasticity and metabolic plasticity.Cell death and differentiation · 2024Review
- The cross talk between type II diabetic microenvironment and the regenerative capacities of human adipose tissue-derived pericytes: a promising cell therapy.Stem cell research & therapy · 2024Article
- Tolerating CD47.Clinical and translational medicine · 2024Review
- The molecular mechanism of thrombospondin family members in cardiovascular diseases.Frontiers in cardiovascular medicine · 2024Review
- Deletion of CD47 from Schwann cells and macrophages hastens myelin disruption/dismantling and scavenging in Schwann cells and augments myelin debris phagocytosis in macrophages.Journal of neuroinflammation · 2023Article
- Matricellular proteins in atherosclerosis development.Matrix biology : journal of the International Society for Matrix Biology · 2023Review
- CD47 antisense oligonucleotide treatment attenuates obesity and its-associated metabolic dysfunction.Scientific reports · 2023Article
- Elevated CD47 is a hallmark of dysfunctional aged muscle stem cells that can be targeted to augment regeneration.Cell stem cell · 2022Article
- ROCK and PDE-5 Inhibitors for the Treatment of Dementia: Literature Review and Meta-Analysis.Biomedicines · 2022Review
- CD47 and thrombospondin-1 regulation of mitochondria, metabolism, and diabetes.American journal of physiology. Cell physiology · 2021Review
- The effects of cell surface CD47 downregulation on ischaemia-reperfusion injury during pig liver transplantation.International journal of experimental pathology · 2021Article
- THBS1 regulates trophoblast fusion through a CD36-dependent inhibition of cAMP, and its upregulation participates in preeclampsia.Genes & diseases · 2021Article
- CD47 (Cluster of Differentiation 47).Atlas of genetics and cytogenetics in oncology and haematology · 2021Article
- Thrombospondin 1 in Metabolic Diseases.Frontiers in endocrinology · 2021Review
- CD47 differentially regulates white and brown fat function.Biology open · 2020Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Nitric oxide (NO) drives pro-survival responses in vascular cells and limits platelet adhesion, enhancing blood flow and minimizing thrombosis. The matricellular protein thrombospondin-1 (TSP1), through interaction with its receptor CD47, inhibits soluble guanylyl cyclase (sGC) activation by NO in vascular cells. In vascular smooth muscle cells (VSMCs) both intracellular cGMP and cAMP regulate adhesion, contractility, proliferation, and migration. cGMP can regulate cAMP through feedback control of hydrolysis. Inhibition of the cAMP phosphodiesterase-4 selectively interfered with the ability of exogenous TSP1 to block NO-driven VSMC adhesion but not cGMP accumulation, suggesting that cAMP also contributes to VSMC regulation by TSP1. Inhibition of phosphodiesterase-4 was sufficient to elevate cAMP levels, and inhibiting guanylyl cyclase or phosphodiesterase-3, or adding exogenous TSP1 reversed this increase in cAMP. Thus, TSP1 regulates VSMC cAMP levels in part via cGMP-dependent inhibition of phosphodiesterase-3. Additionally basal cAMP levels were consistently elevated in both VSMCs and skeletal muscle from TSP1 null mice, and treating null cells with exogenous TSP1 suppressed cAMP levels to those of wild type cells. TSP1 inhibited both forskolin and isoproterenol stimulated increases in cAMP in VSMCs. TSP1 also abrogated forskolin and isoproterenol stimulated vasodilation. Consistent with its ability to directly limit adenylyl cyclase-activated vasodilation, TSP1 also limited cAMP-induced dephosphorylation of myosin light chain-2. These findings demonstrate that TSP1 limits both cGMP and cAMP signaling pathways and functional responses in VSMCs and arteries, by both phosphodiesterase-dependent cross talk between these second messengers and by inhibition of adenylyl cyclase activation.
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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.