ArticleThe Journal of clinical investigation1998
Thrombospondin-1 is required for normal murine pulmonary homeostasis and its absence causes pneumonia.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 202 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
202 citing papers in PubMed, 448 citations in OpenAlex.
- Pro-inflammatory and matricellular protein expression patterns associated with bronchopulmonary dysplasia severity.Pediatric research · 2026Article
- The emerging role of integrin signaling in pulmonary vascular disease.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- Uncovering the Role of Thrombospodin-1 and Occludin as Potential Prognostic and Diagnostic Biomarkers in Traumatic Brain Injury.International journal of molecular sciences · 2026Article
- Herpes simplex virus type-1 ocular infection in thrombospondin-1 deficient C57BL/6J mice.PloS one · 2026Article
- Thrombospondin-1 inhibits alternative complement pathway activation in antineutrophil cytoplasmic antibody-associated vasculitis.The Journal of clinical investigation · 2025Article
- Thrombospondin-1 Airway Expression and Thrombospondin-1 Gene Variants Are Associated with Bronchopulmonary Dysplasia in Extremely Low-Birth-Weight Infants: A Pilot Study.Children (Basel, Switzerland) · 2025Article
- Activation-induced thrombospondin-4 works with thrombospondin-1 to build cytotoxic supramolecular attack particles.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Suppression of thrombospondin-1-mediated inflammaging prolongs hematopoietic health span.Science immunology · 2025Article
- Thrombospondins: Conserved mediators and modulators of metazoan extracellular matrix.International journal of experimental pathology · 2024Review
- Differential regulation by CD47 and thrombospondin-1 of extramedullary erythropoiesis in mouse spleen.eLife · 2024Article
- An isoform quantitative trait locus in SBNO2 links genetic susceptibility to Crohn's disease with defective antimicrobial activity.Nature communications · 2024Article
- Differential regulation by CD47 and thrombospondin-1 of extramedullary erythropoiesis in mouse spleen.bioRxiv : the preprint server for biology · 2024Article
- Thrombospondins modulate cell function and tissue structure in the skeleton.Seminars in cell & developmental biology · 2024Review
- Thrombospondin-1 in vascular development, vascular function, and vascular disease.Seminars in cell & developmental biology · 2024Review
- Spatial transcriptomics reveals novel genes during the remodelling of the embryonic human arterial valves.PLoS genetics · 2023Article
- Why do humans need thrombospondin-1?Journal of cell communication and signaling · 2023Review
- Extracellular Matrix of Echinoderms.Marine drugs · 2023Review
- Ocular Surface Ion Transport and Dry Eye Disease.Current ophthalmology reports · 2022Article
- Bim Expression Modulates Branching Morphogenesis of the Epithelium and Endothelium.Biomolecules · 2022Article
- The matricellular protein thrombospondin-1 in lung inflammation and injury.American journal of physiology. Cell physiology · 2022Review
142 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 5 institutions in 1 country.
Funding
Abstract
The thrombospondins are a family of extracellular calcium-binding proteins that modulate cellular phenotype. Thrombospondin-1 (TSP-1) reportedly regulates cellular attachment, proliferation, migration, and differentiation in vitro. To explore its function in vivo, we have disrupted the TSP-1 gene by homologous recombination in the mouse genome. Platelets from these mice are completely deficient in TSP-1 protein; however, thrombin-induced platelet aggregation is not diminished. TSP-1-deficient mice display a mild and variable lordotic curvature of the spine that is apparent from birth. These mice also display an increase in the number of circulating white blood cells, with monocytes and eosinophils having the largest percent increases. The brain, heart, kidney, spleen, stomach, intestines, aorta, and liver of TSP-1-deficient mice showed no major abnormalities. However, consistent with high levels of expression of TSP-1 in lung, we observe abnormalities in the lungs of mice that lack the protein. Although normal at birth, histopathological analysis of lungs from 4-wk-old TSP-1-deficient mice reveals extensive acute and organizing pneumonia, with neutrophils and macrophages. The macrophages stain for hemosiderin, indicating that diffuse alveolar hemorrhage is occurring. At later times, the number of neutrophils decreases and a striking increase in the number of hemosiderin-containing macrophages is observed associated with multiple-lineage epithelial hyperplasia and the deposition of collagen and elastin. A thickening and ruffling of the epithelium of the airways results from increasing cell proliferation in TSP-1-deficient mice. These results indicate that TSP-1 is involved in normal lung homeostasis.
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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.