ArticlePloS one2011
Mechanical tension increases CCN2/CTGF expression and proliferation in gingival fibroblasts via a TGFβ-dependent mechanism.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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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Who cites it
45 citing papers in PubMed, 83 citations in OpenAlex.
- Gingival Creep Failure: A Viscoelastic Theory of Recession in Thin Periodontal Phenotypes.Biology · 2026Article
- Calcium hydroxyapatite suppresses extracellular matrix-related gene expression by modulating Piezo1-associated CaAnimal cells and systems · 2026Article
- Gli1-expressing stromal cells are highly reparative precursors of long-lived chondroprogenitors in the fetal murine limb.Nature communications · 2025Article
- Effect of mechanical stretching stimulation on maturation of human iPS cell-derived cardiomyocytes co-cultured with human gingival fibroblasts.Scientific reports · 2025Article
- The Areca Nut and Oral Submucosal Fibrosis: A Narrative Review.Dentistry journal · 2025Review
- CTGF (CCN2): a multifaceted mediator in breast cancer progression and therapeutic targeting.Cancer metastasis reviews · 2025Review
- Striking a balance between aesthetics and safety: a comparative study on the maternal and neonatal outcomes of mini-incision cesarean section.BMC pregnancy and childbirth · 2025Article
- Hyperbaric Oxygen Therapy to Minimize Orthodontic Relapse in Rabbits.European journal of dentistry · 2024Article
- Fibrotic pathways and fibroblast-like synoviocyte phenotypes in osteoarthritis.Frontiers in immunology · 2024Review
- Positive Regulation of S-Adenosylmethionine on Chondrocytic Differentiation via Stimulation of Polyamine Production and the Gene Expression of Chondrogenic Differentiation Factors.International journal of molecular sciences · 2023Article
- Rescue of murine hind limb ischemia via angiogenesis and lymphangiogenesis promoted by cellular communication network factor 2.Scientific reports · 2023Article
- Dkk-1-TNF-α crosstalk regulates MC3T3E1 pre-osteoblast proliferation and differentiation under mechanical stress through the ERK signaling pathway.Molecular and cellular biochemistry · 2023Article
- Review
- Drug-Induced Gingival Overgrowth-Molecular Aspects of Drug Actions.International journal of molecular sciences · 2023Review
- Potential Role of CCN Proteins in Breast Cancer: Therapeutic Advances and Perspectives.Current oncology (Toronto, Ont.) · 2021Review
- Functions of Matricellular Proteins in Dental Tissues and Their Emerging Roles in Orofacial Tissue Development, Maintenance, and Disease.International journal of molecular sciences · 2021Review
- CCN2/CTGF promotor activity in the developing and adult mouse eye.Cell and tissue research · 2021Article
- Embryonic protein NODAL regulates the breast tumor microenvironment by reprogramming cancer-derived secretomes.Neoplasia (New York, N.Y.) · 2021Article
- Verteporfin inhibits the persistent fibrotic phenotype of lesional scleroderma dermal fibroblasts.Journal of cell communication and signaling · 2021Article
- CCN2 (Cellular Communication Network factor 2) in the bone marrow microenvironment, normal and malignant hematopoiesis.Journal of cell communication and signaling · 2021Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
Abstract
Unlike skin, oral gingival do not scar in response to tissue injury. Fibroblasts, the cell type responsible for connective tissue repair and scarring, are exposed to mechanical tension during normal and pathological conditions including wound healing and fibrogenesis. Understanding how human gingival fibroblasts respond to mechanical tension is likely to yield valuable insights not only into gingival function but also into the molecular basis of scarless repair. CCN2/connective tissue growth factor is potently induced in fibroblasts during tissue repair and fibrogenesis. We subjected gingival fibroblasts to cyclical strain (up to 72 hours) using the Flexercell system and showed that CCN2 mRNA and protein was induced by strain. Strain caused the rapid activation of latent TGFβ, in a fashion that was reduced by blebbistatin and FAK/src inhibition, and the induction of endothelin (ET-1) mRNA and protein expression. Strain did not cause induction of α-smooth muscle actin or collagen type I mRNAs (proteins promoting scarring); but induced a cohort of pro-proliferative mRNAs and cell proliferation. Compared to dermal fibroblasts, gingival fibroblasts showed reduced ability to respond to TGFβ by inducing fibrogenic mRNAs; addition of ET-1 rescued this phenotype. Pharmacological inhibition of the TGFβ type I (ALK5) receptor, the endothelin A/B receptors and FAK/src significantly reduced the induction of CCN2 and pro-proliferative mRNAs and cell proliferation. Controlling TGFβ, ET-1 and FAK/src activity may be useful in controlling responses to mechanical strain in the gingiva and may be of value in controlling fibroproliferative conditions such as gingival hyperplasia; controlling ET-1 may be of benefit in controlling scarring in response to injury in the skin.
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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.