ArticleMolecular biology of the cell2014
miR-218 regulates focal adhesion kinase-dependent TGFβ signaling in fibroblasts.
Article in Molecular biology of the cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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.
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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
17 citing papers in PubMed, 38 citations in OpenAlex.
- Exploring the complex interplay between oralmSystems · 2025Article
- A Mini-Review on Fibroblast-Derived Exosomes as Wound Healing Stimulators.International journal of hematology-oncology and stem cell research · 2025Review
- Hypoxia macrophage-derived exosomal miR-26b-5p targeting PTEN promotes the development of keloids.Burns & trauma · 2024Article
- Noncoding RNAs: Master Regulator of Fibroblast to Myofibroblast Transition in Fibrosis.International journal of molecular sciences · 2023Review
- Article
- Small extracellular vesicles derived from dermal fibroblasts promote fibroblast activity and skin development through carrying miR-218 and ITGBL1.Journal of nanobiotechnology · 2022Article
- Iron-Dependent Mitochondrial Dysfunction Contributes to the Pathogenesis of Pulmonary Fibrosis.Frontiers in pharmacology · 2021Article
- TGF-β1-induced miR-424 promotes pulmonary myofibroblast differentiation by targeting Slit2 protein expression.Biochemical pharmacology · 2020Article
- In vitro biocompatibility of biohybrid polymers membrane evaluated in human gingival fibroblasts.Journal of biomedical materials research. Part B, Applied biomaterials · 2020Article
- Wound healing and fibrosis: a contrasting role for periostin in skin and the oral mucosa.American journal of physiology. Cell physiology · 2020Review
- Transforming growth factor (TGF)-β1-induced miR-133a inhibits myofibroblast differentiation and pulmonary fibrosis.Cell death & disease · 2019Article
- Increased Expression of MicroRNA 551a by c-Fos Reduces Focal Adhesion Kinase Levels and Blocks Tumorigenesis.Molecular and cellular biology · 2019Article
- Irradiated Human Umbilical Vein Endothelial Cells Undergo Endothelial-Mesenchymal Transition via the Snail/miR-199a-5p Axis to Promote the Differentiation of Fibroblasts into Myofibroblasts.BioMed research international · 2018Article
- Tensile forces drive a reversible fibroblast-to-myofibroblast transition during tissue growth in engineered clefts.Science advances · 2018Article
- Regulation of matrix remodelling phenotype in gingival fibroblasts by substratum topography.Journal of cellular and molecular medicine · 2015Article
- Epithelial Mesenchymal Transition: a double-edged sword.Clinical and translational medicine · 2015Article
- Differential Expression of microRNAs in Thymic Epithelial Cells from Trypanosoma cruzi Acutely Infected Mice: Putative Role in Thymic Atrophy.Frontiers in immunology · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Scarring, which occurs in essentially all adult tissue, is characterized by the excessive production and remodeling of extracellular matrix by α-smooth muscle actin (SMA)-expressing myofibroblasts located within connective tissue. Excessive scarring can cause organ failure and death. Oral gingivae do not scar. Compared to dermal fibroblasts, gingival fibroblasts are less responsive to transforming growth factor β (TGFβ) due to the reduced expression, due to the reduced expression and activity of focal adhesion kinase (FAK) by this cell type. Here we show that, compared with dermal fibroblasts, gingival fibroblasts show reduced expression of miR-218. Introduction of pre-miR-218 into gingival fibroblasts elevates FAK expression and, via a FAK/src-dependent mechanism, results in the ability of TGFβ to induce α-SMA. The deubiquitinase cezanne is a direct target of miR-218 and has increased expression in gingival fibroblasts compared with dermal fibroblasts. Knockdown of cezanne in gingival fibroblasts increases FAK expression and causes TGFβ to induce α-smooth muscle actin (α-SMA). These results suggest that miR-218 regulates the ability of TGFβ to induce myofibroblast differentiation in fibroblasts via cezanne/FAK.
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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.