ArticleBlood2005
Mechanism and effect of thrombospondin-4 polymorphisms on neutrophil function.
Article in Blood, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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Who cites it
24 citing papers in PubMed, 54 citations in OpenAlex.
- Thrombospondin-4 drives lymphangiogenesis through cooperation with VEGF-C in human bladder cancer.International journal of medical sciences · 2026Article
- Pathophysiological roles of thrombospondin-4 in disease development.Seminars in cell & developmental biology · 2024Review
- Gene expression profile of placentomes and clinical parameters in the cows with retained placenta.BMC genomics · 2022Article
- THBS4/integrin α2 axis mediates BM-MSCs to promote angiogenesis in gastric cancer associated with chronicAging · 2021Article
- Thrombospondin-4 promotes bladder cancer cell migration and invasion via MMP2 production.Journal of cellular and molecular medicine · 2021Article
- Thrombospondin-4 induces prolongation of action potential duration in rat isolated ventricular myocytes.The Journal of veterinary medical science · 2020Article
- Effects of thrombospondin-4 on pro-inflammatory phenotype differentiation and apoptosis in macrophages.Cell death & disease · 2020Article
- Thrombospondin-4 in tissue remodeling.Matrix biology : journal of the International Society for Matrix Biology · 2019Review
- Thrombospondins and remodeling of the tumor microenvironment.Vessel plus · 2018Article
- Transcriptome of interstitial cells of Cajal reveals unique and selective gene signatures.PloS one · 2017Article
- Serum stimulation of CCR7 chemotaxis due to coagulation factor XIIa-dependent production of high-molecular-weight kininogen domain 5.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Proangiogenic Properties of Thrombospondin-4.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Effect of donor age on the proportion of mesenchymal stem cells derived from anterior cruciate ligaments.PloS one · 2015Article
- Revisiting the matricellular concept.Matrix biology : journal of the International Society for Matrix Biology · 2014Review
- Invoking the power of thrombospondins: regulation of thrombospondins expression.Matrix biology : journal of the International Society for Matrix Biology · 2014Review
- Thrombospondins: old players, new games.Current opinion in lipidology · 2013Review
- Thrombospondin-4 regulates fibrosis and remodeling of the myocardium in response to pressure overload.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
- Thrombospondins as key regulators of synaptogenesis in the central nervous system.Matrix biology : journal of the International Society for Matrix Biology · 2012Review
- Matricellular proteins in cardiac adaptation and disease.Physiological reviews · 2012Review
- Thrombospondin-4 regulates vascular inflammation and atherogenesis.Circulation research · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
High-throughput genomic technology identified an association between a single nucleotide polymorphism (SNP), a proline (P387) rather than the predominant alanine (A387) at position 387 in thrombospondin-4 (TSP-4) and premature myocardial infarction. The inflammatory hypothesis of atherosclerosis invokes a prominent role of leukocytes and cytokines in pathogenesis. As the expression of TSP-4 by vascular cells permits its exposure to circulating leukocytes, the interactions of human neutrophils (polymorphonuclear leukocytes [PMNs]) with both TSP-4 variants were investigated. Phorbol 12-myristate 13-acetate (PMA)-stimulated PMNs adhered and migrated well and equally on the TSP-4 variants. Integrin alpha(M)beta2 was identified as the TSP-4 receptor mediating these responses, and the 3 epidermal growth factor (EGF)-like domains of TSP-4 harboring the SNPs interacted with the alpha(M)I-domain. Despite the similarity in these responses, the P387 variant induced more robust tyrosine phosphorylation of the stress-related mitogen-activated protein kinases (MAPKs): p38MAPK and c-Jun NH2-terminal kinase (JNK), as well as signal transducer and activator of transcription-1 (STAT1) and heat shock protein 27 (HSP27) than the A387 variant. Additionally, cells adherent to P387 TSP-4 variant released 4-fold more H2O2 and secreted 2-fold more interleukin 8 (IL-8) as compared with the A387. H2O2 release and p38MAPK activation were totally inhibited by blockade of alpha(M)beta2. Thus, alpha(M)beta2 plays a central role in proinflammatory activities of TSP-4 (P387) and may contribute to the prothrombotic phenotype associated with this variant.
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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.