The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Deletion of the alternatively spliced fibronectin EIIIA domain in mice reduces atherosclerosis
Abstract
The alternatively spliced and highly conserved EIIIA domain of fibronectin (FN) is included in most FN of the extracellular matrix in embryos. In adults, both extracellular matrix and plasma FN essentially lack EIIIA. In diverse inflammatory situations however, EIIIA is specifically included by regulated RNA splicing. In atherosclerotic lesions, FN, including the EIIIA domain (EIIIA-FN), is abundant, whereas FN in the flanking vessel wall lacks EIIIA. Lesional EIIIA-FN is localized with endothelial cells and macrophage foam cells. To directly test the function of EIIIA-FN, we generated EIIIA-null (EIIIA–/–) mice that lack the EIIIA exon and crossed them with apolipoprotein E (ApoE)–null (ApoE–/–) mice that develop arterial wall lesions. Compared with ApoE–/– controls, EIIIA–/–ApoE–/– mice had significantly smaller lesions throughout the aortic tree. EIIIA-FN was increased in ApoE–/– plasma, and total plasma cholesterol was reduced in EIIIA–/–ApoE–/– mice, specifically in large lipoprotein particles, suggesting a functional role for plasma EIIIA-FN. To assess a role for macrophage EIIIA-FN in the vessel wall, we conducted in vitro foam cell assays. EIIIA–/–ApoE–/– macrophages accumulated significantly less intracellular lipid than control ApoE–/– cells. These results provide genetic evidence that suggests roles for EIIIA-FN in plasma lipoprotein metabolism and in foam cell formation.
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The interplay of fibroblasts, the extracellular matrix, and inflammation in scar formation
Moretti, L., Stalfort, J., Barker, T. H., & Abebayehu, D. (2022) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2021.101530 · Cited by 393
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Metadata
- Authors
- Tan, M. H., Sun, Z., Opitz, S. L., Schmidt, T. E., Peters, J. H., & George, E. L.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2004-07-01
- Volume
- 104
- Issue
- 1
- Pages
- 11-18
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2010791052
- Cited by
- 178
- References
- 7
- FWCI
- 5.67
- Type
- journal article
- Language
- en
- Open access
- closed
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- Tan, M. H., Sun, Z., Opitz, S. L., Schmidt, T. E., Peters, J. H., & George, E. L. (2004). Deletion of the alternatively spliced fibronectin EIIIA domain in mice reduces atherosclerosis. Blood. https://doi.org/10.1182/blood-2003-09-3363
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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