ArticleMediators of inflammation2005
Suppression of matrix metalloproteinase production in nasal fibroblasts by tranilast, an antiallergic agent, in vitro.
Article in Mediators of inflammation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 30 citations in OpenAlex.
- Tranilast Modulates Cellular and Matrix Remodeling in Achilles Tendon Healing: A Comprehensive Histological and Biomechanical Analysis.Bioengineering (Basel, Switzerland) · 2026Article
- Tranilast Treatment Prevents Chronic Radiation-Induced Colitis in Rats by Inhibiting Mast Cell Infiltration.Pharmacology · 2025Article
- The Presence and Severity of Inferior Turbinate Hypertrophy in Patients with Hypertrophic Scars.Sisli Etfal Hastanesi tip bulteni · 2024Article
- Role of Nasal Fibroblasts in Airway Remodeling of Chronic Rhinosinusitis: The Modulating Functions Reexamined.International journal of molecular sciences · 2023Review
- Serum level and clinical significance of vitamin E in pregnant women with allergic rhinitis.Journal of the Chinese Medical Association : JCMA · 2022Article
- A novel mice model of acute flares in osteoarthritis elicited by intra-articular injection of cultured mast cells.Journal of experimental orthopaedics · 2021Article
- Inhibition of transforming growth factor-beta by Tranilast reduces tumor growth and ameliorates fibrosis in colorectal cancer.EXCLI journal · 2021Article
- Evaluation of cationic channel TRPV2 as a novel biomarker and therapeutic target in Leukemia-Implications concerning the resolution of pulmonary inflammation.Scientific reports · 2019Article
- Anti-allergic effect of the naturally-occurring conjugated linolenic acid isomer, jacaric acid, on the activated human mast cell line-1.Biomedical reports · 2015Article
- The effect of environmental chemicals on the tumor microenvironment.Carcinogenesis · 2015Review
- Tranilast administration reduces fibrosis and improves fatigue resistance in muscles of mdx dystrophic mice.Fibrogenesis & tissue repair · 2014Article
- Expression and Roles of MMP-2, MMP-9, MMP-13, TIMP-1, and TIMP-2 in Allergic Nasal Mucosa.Allergy, asthma & immunology research · 2012Article
- Mast cells and MMP-9 in the lamina propria during eruption of rat molars: quantitative and immunohistochemical evaluation.Journal of anatomy · 2010Article
- The anti-allergic compound tranilast attenuates inflammation and inhibits bone destruction in collagen-induced arthritis in mice.British journal of pharmacology · 2010Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Allergic rhinitis is an inflammatory disease characterized by nasal wall remodeling with intense infiltration of eosinophils and mast cells/basophils. Matrix metalloproteinases (MMPs), MMP-2 and MMP-9, are the major proteolytic enzymes that induce airway remodeling. These enzymes are also important in the migration of inflammatory cells through basement membrane components. We evaluated whether tranilast (TR) could inhibit MMP production from nasal fibroblasts in response to tumor necrosis factor-alpha (TNF-alpha) stimulation in vitro. Nasal fibroblasts (NF) were established from nasal polyp tissues taken from patients with allergic rhinitis. NF (2 x 10(5) cells/mL) were stimulated with TNF-alpha in the presence of various concentrations of TR. After 24 hours, the culture supernatants were obtained and assayed for MMP-2, MMP-9, TIMP-1, and TIMP-2 levels by ELISA. The influence of TR on mRNA expression of MMPs and TIMPs in cells cultured for 12 hours was also evaluated by RT-PCR. TR at more than 5 x 10(-5) M inhibited the production of MMP-2 and MMP-9 from NF in response to TNF-alpha stimulation, whereas TIMP-1 and TIMP-2 production was scarcely affected. TR also inhibited MMP mRNA expression in NF after TNF-alpha stimulation. The present data suggest that the attenuating effect of TR on MMP-2 and MMP-9 production from NF induced by inflammatory stimulation may underlie the therapeutic mode of action of the agent in patients with allergic diseases, including allergic rhinitis.
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