ArticleThe American journal of pathology2010
Dermal transforming growth factor-beta responsiveness mediates wound contraction and epithelial closure.
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 42 papers, 1 of them a synthesis that pooled it.
What it found
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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
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- Transcriptomic responses to wounding: meta-analysis of gene expression microarray data.BMC genomics · 2017Pooled it
- Adipose-Derived Stem Cell Exosomes in Diabetic Wound Repair: Molecular Crosstalk, Bioengineering Strategies, and Translational Challenges.Stem cells international · 2026Review
- Improving the Culture of Human Skin Explants for Use in Preclinical Testing of Wound Healing Treatments.Pharmaceutics · 2025Article
- Article
- Mesenchymal stem cells and their exosomes: a novel approach to skin regeneration via signaling pathways activation.Journal of molecular histology · 2025Review
- Assessment ofBiomolecules · 2024Article
- TEM1/endosialin/CD248 promotes pathologic scarring and TGF-β activity through its receptor stability in dermal fibroblasts.Journal of biomedical science · 2024Article
- Hair-follicle associated pluripotent (HAP)-cell-sheet implantation enhanced wound healing in diabetic db/db mice.PloS one · 2024Article
- Therapeutic role of growth factors in treating diabetic wound.World journal of diabetes · 2023Review
- Macrophage Phenotypes in Normal and Diabetic Wound Healing and Therapeutic Interventions.Cells · 2022Review
- Phospholipid-grafted PLLA electrospun micro/nanofibers immobilized with small extracellular vesicles from rat adipose mesenchymal stem cells promote wound healing in diabetic rats.Regenerative biomaterials · 2022Article
- Novel lipophosphonoxin-loaded polycaprolactone electrospun nanofiber dressing reduces Staphylococcus aureus induced wound infection in mice.Scientific reports · 2021Article
- Interplay between Cell-Surface Receptors and Extracellular Matrix in Skin.Biomolecules · 2020Review
- Review
- Article
- Low Degree Hyaluronic Acid Crosslinking Inducing the Release of TGF-Β1 in Conditioned Medium of Wharton's Jelly-Derived Stem Cells.Open access Macedonian journal of medical sciences · 2019Article
- α-Ionone Protects Against UVB-Induced Photoaging in Human Dermal Fibroblasts.Molecules (Basel, Switzerland) · 2019Article
- Natural Selection Equally Supports the Human Tendencies in Subordination and Domination: A Genome-Wide Study WithFrontiers in genetics · 2019Article
- Vascular endothelial Cdc42 deficiency delays skin wound-healing processes by increasing IL-1β and TNF-α expression.American journal of translational research · 2019Article
- Scar management in burn injuries using drug delivery and molecular signaling: Current treatments and future directions.Advanced drug delivery reviews · 2018Review
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
Stromal-epithelial interactions are important during wound healing. Transforming growth factor-beta (TGF-beta) signaling at the wound site has been implicated in re-epithelization, inflammatory infiltration, wound contraction, and extracellular matrix deposition and remodeling. Ultimately, TGF-beta is central to dermal scarring. Because scarless embryonic wounds are associated with the lack of dermal TGF-beta signaling, we studied the role of TGF-beta signaling specifically in dermal fibroblasts through the development of a novel, inducible, conditional, and fibroblastic TGF-beta type II receptor knockout (Tgfbr2(dermalKO)) mouse model. Full thickness excisional wounds were studied in control and Tgfbr2(dermalKO) back skin. The Tgfbr2(dermalKO) wounds had accelerated re-epithelization and closure compared with controls, resurfacing within 4 days of healing. The loss of TGF-beta signaling in the dermis resulted in reduced collagen deposition and remodeling associated with a reduced extent of wound contraction and elevated macrophage infiltration. Tgfbr2(dermalKO) and control skin had similar numbers of myofibroblastic cells, suggesting that myofibroblastic differentiation was not responsible for reduced wound contraction. However, several mediators of cell-matrix interaction were reduced in the Tgfbr2(dermalKO) fibroblasts, including alpha1, alpha2, and beta1 integrins, and collagen gel contraction was diminished. There were associated deficiencies in actin cytoskeletal organization of vasodilator-stimulated phosphoprotein-containing lamellipodia. This study indicated that paracrine and autocrine TGF-beta dermal signaling mechanisms mediate macrophage recruitment, re-epithelization, and wound contraction.
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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.