ArticleAtherosclerosis2013
Tenascin-C deficiency in apo E-/- mouse increases eotaxin levels: implications for atherosclerosis.
Article in Atherosclerosis, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 14 citations in OpenAlex.
- Bioactive TNIIIA2 Sequence in Tenascin-C Is Responsible for Macrophage Foam Cell Transformation; Potential of FNIII14 Peptide Derived from Fibronectin in Suppression of Atherosclerotic Plaque Formation.International journal of molecular sciences · 2024Article
- The role of TNC in atherosclerosis and drug development opportunities.International journal of biological sciences · 2024Review
- Matricellular proteins in atherosclerosis development.Matrix biology : journal of the International Society for Matrix Biology · 2023Review
- Article
- The Roles of Tenascins in Cardiovascular, Inflammatory, and Heritable Connective Tissue Diseases.Frontiers in immunology · 2020Review
- Multiple Roles of Tenascins in Homeostasis and Pathophysiology of Aorta.Annals of vascular diseases · 2018Article
- Tenascin-c renders a proangiogenic phenotype in macrophage via annexin II.Journal of cellular and molecular medicine · 2018Article
- Oxidized LDL activated eosinophil polarize macrophage phenotype from M2 to M1 through activation of CD36 scavenger receptor.Atherosclerosis · 2017Article
- Clinical relevance of gemstone spectral CT in the diagnosis of carotid atherosclerosis.Experimental and therapeutic medicine · 2017Article
- Diagnostic potential of differentially expressed Homer1, IL-1β, and TNF-α in coronary artery disease.International journal of molecular sciences · 2014Article
- Article
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 2 institutions in 1 country.
Funding
Abstract
aimTo investigate the potential role of inflammatory cytokines in apo E-/- mouse in response to deletion of Tenascin-C (TNC) gene. METHODS AND
resultsWe used antibody array and ELISA to compare the profile of circulating inflammatory cytokines in apo E-/- mice and apo E-/- TNC-/- double knockout mice. In addition, tissue culture studies were performed to investigate the activity of cells from each mouse genotype in vitro. Cytokine array analysis and subsequent ELISA showed that circulating eotaxin levels were selectively and markedly increased in response to TNC gene deletion in apo E-/- mice. In addition, considerable variation was noted in the circulating level of eotaxin among the control apo E-/- mouse group. Inbreeding of apo E-/- mice with high or low levels of plasma eotaxin showed that the level of eotaxin per se determines the extent of atherosclerosis in this mouse genotype. While endothelial cells from apo E-/- mice had low level of eotaxin expression, cells derived from apo E-/- TNC-/- mice expressed a high level of eotaxin. Transient transfection of eotaxin promoter-reporter constructs revealed that eotaxin expression is regulated at the transcriptional level by TNC. Histochemical analysis of aortic sections revealed the massive accumulation of mast cells in the adventitia of double KO mice lesions whereas no such accumulation was detected in the control group. Plasma from the apo E-/- TNC-/- mice markedly stimulated mast cell migration whereas plasma from the apo E-/- mice had no such effect.
conclusionThese observations support the emerging hypothesis that TNC expression controls eotaxin level in apo E-/- mice and that this chemokine plays a key role in the development of atherosclerosis.
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.