ArticleMethods in molecular biology (Clifton, N.J.)2021
Myofibroblast TGF-β Activation Measurement In Vitro.
Article in Methods in molecular biology (Clifton, N.J.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Mathematical Modeling of Systemic Sclerosis and Its Treatment.Bulletin of mathematical biology · 2026Article
- Ferroptosis in idiopathic pulmonary fibrosis: mechanisms, impact, and therapeutic opportunities.Frontiers in immunology · 2025Review
- Botulinum toxin type A inhibits the formation of hypertrophic scar through the JAK2/STAT3 pathway.Biomolecules & biomedicine · 2024Article
- Nintedanib downregulates the profibrotic M2 phenotype in cultured monocyte-derived macrophages obtained from systemic sclerosis patients affected by interstitial lung disease.Arthritis research & therapy · 2024Article
- Integrins as a bridge between bacteria and cells: key targets for therapeutic wound healing.Burns & trauma · 2024Review
- Direct cellular reprogramming and transdifferentiation of fibroblasts on wound healing-Fantasy or reality?Chronic diseases and translational medicine · 2023Review
- The Interplay between Integrins and Immune Cells as a Regulator in Cancer Immunology.International journal of molecular sciences · 2023Review
- Targeting integrin pathways: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2023Review
- Association between Immunologic Markers and Cirrhosis in Individuals from a Prospective Chronic Hepatitis C Cohort.Cancers · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myofibroblasts are critical to processes involved in normal wound healing and during pathological fibrosis. They transdifferentiate from fibroblasts, and in doing so become contractile and capable of secreting large amounts of extracellular matrix proteins. Transforming growth factor-beta (TGFβ) is a key cytokine involved in wound healing and fibrogenesis. TGFβ signaling has long been the subject of experimental therapeutic approaches to inhibit fibrosis in a variety of organ systems. Inhibition of TGFβ can reduce myofibroblast transdifferentiation, contractility, and matrix production. Importantly, TGFβ is released from cells and sequestered in the extracellular matrix in a latent form that requires activation for biological function. There have been multiple mechanisms of TGFβ activation described in a variety of cell types and in cell free systems; however, myofibroblasts have previously been shown to activate TGFβ via cell surface integrins, particularly αvβ5 integrins. This chapter will provide detailed protocols for accurately measuring activation of TGFβ by myofibroblasts in vitro. Levels of active TGFβ usually represent a small proportion of the total amount of latent TGFβ present in the matrix. Methods to measure active TGFβ therefore need to be sensitive and specific to detect the active cytokine only.
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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.