ArticleScientific reports2023
Substrate stiffness controls proinflammatory responses in human gingival fibroblasts.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 20 citations in OpenAlex.
- Mechanobiology of orofacial tissues: principles, mechanisms, and therapeutic applications.International journal of oral science · 2026Review
- Matrix Stiffness Drives Aggressive Phenotype in Tongue Squamous Cell Carcinoma via Mechanotransduction-Stromal Signalling.International dental journal · 2026Article
- Dental implant nanotopography for peri-implant tissue stability: soft-tissue sealing, innate immune calibration, and active biointerface regulation.International journal of implant dentistry · 2026Review
- Matrix viscoelasticity regulates dermal fibroblast activation in a three-dimensional fibrillar microenvironment.bioRxiv : the preprint server for biology · 2026Article
- Matrix Stiffness Governs Fibroblasts' Regulation of Gingival Immune Homeostasis.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Substrate elasticity controls fibroblast motility on non-oxidized PDMS under weak adhesion.Biophysics and physicobiology · 2026Article
- Exploring Matrix Stiffness-Related Gene in Periodontitis: A Comprehensive Multidataset Analysis.Mediators of inflammation · 2026Article
- Mechanical forces orchestrate the epigenetic landscape of oral mesenchymal stem/progenitor cell fate in dental and periodontal tissues.Frontiers in cell and developmental biology · 2026Review
- Substrate stiffness modulates human gingival fibroblast paracrine signaling to promote osteogenic differentiation of human periodontal ligament cells.Frontiers in bioengineering and biotechnology · 2026Article
- Biomolecule-functionalized dental implant surfaces: Towards augmenting soft tissue integration.Bioactive materials · 2025Review
- Matrix Stiffness Governs Fibroblast-Driven Immune Homeostasis in Gingival Tissues.bioRxiv : the preprint server for biology · 2025Article
- Utilising Human Myometrial and Uterine Fibroid Stem Cell-Derived Three Dimentional Organoids as a Robust Model System for Understanding the Pathophysiology of Uterine Fibroids.Cell proliferation · 2025Article
- The Rise of Mechanobiology for Advanced Cell Engineering and Manufacturing.Advanced materials (Deerfield Beach, Fla.) · 2025Review
- Review
- Biophysical aspects of mechanotransduction in cells and their physiological/biological implications in vocal fold vibration: a narrative review.Frontiers in cell and developmental biology · 2025Review
- Article
- Vaginal Fibroblast Behavior as a Function of Stiffness Changes in a Polyisocyanide Hydrogel for Prolapse Repair.ACS applied bio materials · 2023Article
- Incomplete Polymerization of Dual-Cured Resin Cement Due to Attenuated Light through Zirconia Induces Inflammatory Responses.International journal of molecular sciences · 2023Article
- Mechanoregulation of Osteoclastogenesis-Inducing Potentials of Fibrosarcoma Cell Line by Substrate Stiffness.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Soft gingiva is often compromised in gingival health; however, the underlying biological mechanisms remain unknown. Extracellular matrix (ECM) stiffness is involved in the progression of various fibroblast-related inflammatory disorders via cellular mechanotransduction. Gingival stiffness might regulate cellular mechanotransduction-mediated proinflammatory responses in gingival fibroblasts. This in vitro study aims to investigate the effects of substrate stiffness on proinflammatory responses in human gingival fibroblasts (hGFs). The hGFs isolated from two healthy donors cultured on type I collagen-coated polydimethylsiloxane substrates with different stiffnesses, representing soft (5 kPa) or hard (25 kPa) gingiva. Expression levels of proinflammatory mediators, prostaglandin E2 or interleukin-1β, in hGFs were significantly higher with the soft substrate than with the hard substrate, even without and with lipopolysaccharide (LPS) to induce inflammation. Expression levels of gingival ECM and collagen cross-linking agents in hGFs were downregulated more with the soft substrate than with the hard substrate through 14 days of culture. The soft substrate suppressed the expression of mechanotransduction-related transcriptional factors and activated the expression of inflammation-related factors, whereas the hard substrate demonstrated the opposite effects. Soft substrate induced proinflammatory responses and inhibition of ECM synthesis in hGFs by inactivating cellular mechanotransduction. This supports the importance of ECM stiffness in gingival health.
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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.