ArticleStem cells (Dayton, Ohio)2012
Injury-activated transforming growth factor β controls mobilization of mesenchymal stem cells for tissue remodeling.
Article in Stem cells (Dayton, Ohio), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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Who cites it
90 citing papers in PubMed, 143 citations in OpenAlex.
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- Signaling Pathways Driving MSC Osteogenesis: Mechanisms, Regulation, and Translational Applications.International journal of molecular sciences · 2025Review
- Differentiation of stem cells into chondrocytes and their potential clinical application in cartilage regeneration.Histochemistry and cell biology · 2025Review
- Extracellular vesicles therapy alleviates cisplatin-ınduced testicular tissue toxicity in a rat model.PloS one · 2025Article
- Animal models of tendon calcification: Past, present, and future.Animal models and experimental medicine · 2024Review
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- Sphingolipid-Induced Bone Regulation and Its Emerging Role in Dysfunction Due to Disease and Infection.International journal of molecular sciences · 2024Review
- A comparative study on the effects of biodegradable high-purity magnesium screw and polymer screw for fixation in epiphyseal trabecular bone.Regenerative biomaterials · 2024Article
- Effect of Expansion Media on Functional Characteristics of Bone Marrow-Derived Mesenchymal Stromal Cells.Cells · 2023Article
- Neutralization of excessive levels of active TGF-β1 reduces MSC recruitment and differentiation to mitigate peritendinous adhesion.Bone research · 2023Article
- Correlation between stem cell molecular phenotype and atherosclerotic plaque neointima formation and analysis of stem cell signal pathways.Frontiers in cell and developmental biology · 2023Review
- TGF-β1-induced bone marrow mesenchymal stem cells (BMSCs) migration via histone demethylase KDM6B mediated inhibition of methylation marker H3K27me3.Cell death discovery · 2022Article
- Blood Vessel Resident Human Stem Cells in Health and Disease.Stem cells translational medicine · 2022Review
- BATF promotes group 2 innate lymphoid cell-mediated lung tissue protection during acute respiratory virus infection.Science immunology · 2022Article
- Exosomal Composition, Biogenesis and Profiling Using Point-of-Care Diagnostics-Implications for Cardiovascular Disease.Frontiers in cell and developmental biology · 2022Review
- Mechanical Stimulation on Mesenchymal Stem Cells and Surrounding Microenvironments in Bone Regeneration: Regulations and Applications.Frontiers in cell and developmental biology · 2022Review
- Periosteal CD68Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Cell autonomous TGFβ signaling is essential for stem/progenitor cell recruitment into degenerative tendons.Stem cell reports · 2021Article
- Article
30 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Upon secretion, transforming growth factor β (TGFβ) is maintained in a sequestered state in extracellular matrix as a latent form. The latent TGFβ is considered as a molecular sensor that releases active TGFβ in response to the perturbations of the extracellular matrix at the situations of mechanical stress, wound repair, tissue injury, and inflammation. The biological implication of the temporal discontinuity of TGFβ storage in the matrix and its activation is obscure. Here, using several animal models in which latent TGFβ is activated in vascular matrix in response to injury of arteries, we show that active TGFβ controls the mobilization and recruitment of mesenchymal stem cells (MSCs) to participate in tissue repair and remodeling. MSCs were mobilized into the peripheral blood in response to vascular injury and recruited to the injured sites where they gave rise to both endothelial cells for re-endothelialization and myofibroblastic cells to form thick neointima. TGFβs were activated in the vascular matrix in both rat and mouse models of mechanical injury of arteries. Importantly, the active TGFβ released from the injured vessels is essential to induce the migration of MSCs, and cascade expression of monocyte chemotactic protein-1 stimulated by TGFβ amplifies the signal for migration. Moreover, sustained high levels of active TGFβ were observed in peripheral blood, and at the same time points following injury, Sca1+ CD29+ CD11b- CD45- MSCs, in which 91% are nestin+ cells, were mobilized to peripheral blood and recruited to the remodeling arteries. Intravenously injection of recombinant active TGFβ1 in uninjured mice rapidly mobilized MSCs into circulation. Furthermore, inhibitor of TGFβ type I receptor blocked the mobilization and recruitment of MSCs to the injured arteries. Thus, TGFβ is an injury-activated messenger essential for the mobilization and recruitment of MSCs to participate in tissue repair/remodeling.
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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.