ArticleInternational journal of biological sciences2015
Activation of TLR3 induces osteogenic responses in human aortic valve interstitial cells through the NF-κB and ERK1/2 pathways.
Article in International journal of biological sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- Sodium-Glucose Cotransporter 2 Inhibitors in Aortic Stenosis: Toward a Comprehensive Cardiometabolic Approach.International journal of molecular sciences · 2025Review
- The role of ERK1/2 signaling in diabetes: pathogenic and therapeutic implications.Frontiers in pharmacology · 2025Review
- Inducing cyclooxygenase-2 expression, prostaglandin EJournal of dental sciences · 2024Article
- Molecular Interaction of Soluble Klotho with FGF23 in the Pathobiology of Aortic Valve Lesions Induced by Chronic Kidney Disease.International journal of biological sciences · 2024Article
- Similarities and Differences of Vascular Calcification in Diabetes and Chronic Kidney Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Inflammation-associated ectopic mineralization.Fundamental research · 2023Review
- Toll-Like Receptor 3 Mediates Aortic Stenosis Through a Conserved Mechanism of Calcification.Circulation · 2023Article
- Toll-like receptor-3 contributes to the development of aortic valve stenosis.Basic research in cardiology · 2023Article
- A long non-coding RNA H19/microRNA-138/TLR3 network is involved in high phosphorus-mediated vascular calcification and chronic kidney disease.Cell cycle (Georgetown, Tex.) · 2022Article
- Warfarin Induces Calcification of the Aortic Valve Through Extracellular Signal-regulated Kinase 1/2 and β-catenin Signaling.The Annals of thoracic surgery · 2022Article
- Pro-inflammatory mediators released by activated monocytes promote aortic valve fibrocalcific activity.Molecular medicine (Cambridge, Mass.) · 2022Article
- MyD88: At the heart of inflammatory signaling and cardiovascular disease.Journal of molecular and cellular cardiology · 2021Review
- MyD88 Is Not Required for Muscle Injury-Induced Endochondral Heterotopic Ossification in a Mouse Model of Fibrodysplasia Ossificans Progressiva.Biomedicines · 2021Article
- The Role of NLRP3 Inflammasome Activities in Bone Diseases and Vascular Calcification.Inflammation · 2021Review
- Tumor necrosis factor-α promotes and exacerbates calcification in heart valve myofibroblast populations.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Clonal haematopoiesis in patients with degenerative aortic valve stenosis undergoing transcatheter aortic valve implantation.European heart journal · 2020Article
- Monocytes enhance the inflammatory response to TLR2 stimulation in aortic valve interstitial cells through paracrine up-regulation of TLR2 level.International journal of biological sciences · 2020Article
- Optimal antithrombotic therapy after transcatheter aortic valve replacement in patients with atrial fibrillation.Therapeutic advances in chronic disease · 2020Review
- Involvement of inflammatory responses in the early development of calcific aortic valve disease: lessons from statin therapy.Animal cells and systems · 2018Review
- Advances in Pathophysiology of Calcific Aortic Valve Disease Propose Novel Molecular Therapeutic Targets.Frontiers in cardiovascular medicine · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
unlabelledCalcific aortic valve disease (CAVD) is characterized by chronic inflammation and progressive calcification in valve leaflets. Aortic valve interstitial cells (AVICs) play a critical role in the pathogenesis of CAVD. Previous studies show that stimulation of Toll-like receptor (TLR) 2 or TLR4 in AVICs in vitro up-regulates the expression of osteogenic mediators. Double-stranded RNA (dsRNA) can activate pro-inflammatory signaling through TLR3, the NLRP3 inflammasome and RIG-I-like receptors. The objective of this study is to determine the effect of dsRNA on AVIC osteogenic activities and the mechanism of its action. METHODS AND
resultsAVICs isolated from normal human valves were exposed to polyinosinic-polycytidylic acid [poly(I:C)], a mimic of dsRNA. Treatment with poly(I:C) increased the production of bone morphogenetic protein-2 (BMP-2), transforming growth factor beta-1 (TGF-β1) and alkaline phosphatase (ALP), and resulted in calcium deposit formation. Poly(I:C) induced the phosphorylation of NF-κB and ERK1/2. Knockdown of TLR3 essentially abrogated NF-κB and ERK1/2 phosphorylation, and markedly reduced the effect of poly(I:C) on the production of BMP-2, TGF-β1 and ALP. Further, inhibition of either NF-κB or ERK1/2 markedly reduced the levels of BMP-2, TGF-β1 and ALP in cells exposed to poly(I:C).
conclusionPoly(I:C) up-regulates the production of BMP-2, TGF-β1 and ALP, and promotes calcium deposit formation in human AVICs. The pro-osteogenic effect of poly(I:C) is mediated primarily by TLR3 and the NF-κB and ERK1/2 pathways. These findings suggest that dsRNA, when present in aortic valve tissue, may promote CAVD progression through up-regulation of AVIC osteogenic activities.
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