ArticleThe American journal of pathology2010
Left-sided cardiac valvulitis in tristetraprolin-deficient mice: the role of tumor necrosis factor alpha.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Multi-species meta-analysis identifies transcriptional signatures associated with cardiac endothelial responses in the ischaemic heart.Cardiovascular research · 2023Pooled it
- Lymphatic dysfunction and ZFP36 deficiency contribute to myxomatous valve degeneration in Marfan syndrome mice.The Journal of clinical investigation · 2026Article
- Synergistic roles of tristetraprolin family members in myeloid cells in the control of inflammation.Life science alliance · 2024Article
- Cardiovascular inflammation: RNA takes the lead.Journal of molecular and cellular cardiology · 2019Review
- Cardiac phenotype in mouse models of systemic autoimmunity.Disease models & mechanisms · 2019Review
- Comorbid TNF-mediated heart valve disease and chronic polyarthritis share common mesenchymal cell-mediated aetiopathogenesis.Annals of the rheumatic diseases · 2018Article
- Mesenchymal TNFR2 promotes the development of polyarthritis and comorbid heart valve stenosis.JCI insight · 2018Article
- A Knock-In Tristetraprolin (TTP) Zinc Finger Point Mutation in Mice: Comparison with Complete TTP Deficiency.Molecular and cellular biology · 2018Article
- Tristetraprolin (TTP) coordinately regulates primary and secondary cellular responses to proinflammatory stimuli.Journal of leukocyte biology · 2015Article
- Endothelial dysfunction in tristetraprolin-deficient mice is not caused by enhanced tumor necrosis factor-α expression.The Journal of biological chemistry · 2014Article
- Post-transcriptional control of cytokine gene expression in health and disease.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014Article
- Tristetraprolin expression and microRNA-mediated regulation during simian immunodeficiency virus infection of the central nervous system.Molecular brain · 2013Article
- Myeloid-specific tristetraprolin deficiency in mice results in extreme lipopolysaccharide sensitivity in an otherwise minimal phenotype.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Recruitment of bone marrow-derived valve interstitial cells is a normal homeostatic process.Journal of molecular and cellular cardiology · 2011Article
- Zinc finger protein tristetraprolin interacts with CCL3 mRNA and regulates tissue inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- The roles of TTP and BRF proteins in regulated mRNA decay.Wiley interdisciplinary reviews. RNAReview
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Inflammation may play a role in the etiology of both degenerative and rheumatic cardiac valve diseases. We report here that mice deficient in tristetraprolin (TTP), a protein with known anti-inflammatory functions, develop severe left-sided cardiac valvulitis. TTP is an mRNA binding protein that inhibits inflammation by destabilizing the mRNA encoding tumor necrosis factor alpha (TNF). This leads in turn to a TNF-excess syndrome characterized by systemic inflammation. Evaluation of hearts from TTP-/- mice demonstrated gross thickening of the mitral and aortic but not the tricuspid or pulmonary valves, accompanied by inflammatory cell infiltrates. To determine whether TNF played a role in the development of this valvulitis, we examined mice deficient in both TNF receptors and in TTP; four of five of these mice exhibited no histological evidence of valvulitis, but one mouse had aortic valve leaflet thickening with a cellular infiltrate. Four additional mice had no external evidence of valvular thickening. Cardiac valves of transgenic mice expressing human TNF developed mild aortic valve leaflet edema without evidence of hypercellularity. Thus, TTP deficiency in mice leads to left-sided cardiac valvulitis with prominent inflammatory cell involvement, due, at least in part, to excess TNF. These findings support the potential involvement of TNF and inflammation in the development of cardiac valve disease in man.
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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.