ArticleMediators of inflammation2004
Expression of nitric oxide synthase and transforming growth factor-beta in crush-injured tendon and synovium.
Article in Mediators of inflammation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Profibrotic mediators in tendon disease: a systematic review.Arthritis research & therapy · 2016Pooled it
- MicroRNA-29a Exhibited Pro-Angiogenic and Anti-Fibrotic Features to Intensify Human Umbilical Cord Mesenchymal Stem Cells-Renovated Perfusion Recovery and Preventing against Fibrosis from Skeletal Muscle Ischemic Injury.International journal of molecular sciences · 2019Article
- Human Umbilical Cord Mesenchymal Stem Cells Extricate Bupivacaine-Impaired Skeletal Muscle Function via Mitigating Neutrophil-Mediated Acute Inflammation and Protecting against Fibrosis.International journal of molecular sciences · 2019Article
- Stem cell activation in skeletal muscle regeneration.Cellular and molecular life sciences : CMLS · 2015Review
- Satellite cells and the muscle stem cell niche.Physiological reviews · 2013Review
- The role of nitric oxide during healing of trauma to the skeletal muscle.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2011Article
- Nonsteroidal anti-inflammatory drugs for wounds: pain relief or excessive scar formation?Mediators of inflammation · 2010Review
- Spatiotemporal protein distribution of TGF-betas, their receptors, and extracellular matrix molecules during embryonic tendon development.Developmental dynamics : an official publication of the American Association of Anatomists · 2008Article
- The inflammatory response to skeletal muscle injury: illuminating complexities.Sports medicine (Auckland, N.Z.) · 2008Review
- Nutraceutical supplement in the management of tendinopathies: a systematic review.Muscles, ligaments and tendons journalReview
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study examined the expression of inducible nitric oxide synthase (iNOS) and transforming growth factor-beta (TGF-beta) in macrophage infiltrates within crush-injured digital flexor tendon and synovium of control rats and rats treated with N(G)-nitro-1-arginine methyl ester (L-NAME) (5 mg/kg). Release of TGF-beta from organ cultures of tendon, muscle, and synovium, and the effects of L-NAME treatment (in vitro and in vivo), on adhesion of peritoneal macrophages to epitenon monolayers were also investigated. The results showed that during normal tendon healing the levels of TGF-beta are high at first and gradually decrease after 3 weeks of injury to slightly above control uninjured levels. However, when L-NAME was administered at the time of injury, the macrophage infiltrates were expressing high levels of TGF-beta even at 5 weeks after the injury, with no evidence of reduction. In the standard injury, iNOS activity was greatest at the acute phase of the inflammatory response and then gradually returned to normal. Treatment with L-NAME, however, resulted in inhibition of iNOS activity at 3 days and a reduction in the activity at the later time points examined after injury. We also found greatly increased levels of adhesion of peritoneal macrophages from L-NAME-treated rats to epitenon monolayers in vitro, which reflect a chronic imbalance in expression of TGF-beta, which is overexpressed, and nitric oxide, which is underexpressed. The results of the current study show that formation of nitric oxide is an important event in the course of tendon healing since its inhibition results in chronic inflammation and fibrosis due to an imbalance in TGF-beta expression in vivo.
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