ArticlePloS one2015
Inhibition of T-Type Voltage Sensitive Calcium Channel Reduces Load-Induced OA in Mice and Suppresses the Catabolic Effect of Bone Mechanical Stress on Chondrocytes.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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
22 citing papers in PubMed, 34 citations in OpenAlex.
- The regulatory significance of chondrocyte hypertrophy in maintaining chondrocyte homeostasis, regeneration and repair.Future science OA · 2026Review
- Ion channels as therapeutic targets in osteoarthritis.Trends in pharmacological sciences · 2025Review
- Genetic fine-mapping of body weight and size traits at 120 days of age in Lion-head geese.BMC genomics · 2025Article
- The cartilage-generated bioelectric potentials induced by dynamic joint movement; an exploratory study.BMC musculoskeletal disorders · 2025Article
- Ion channels in osteoarthritis: emerging roles and potential targets.Nature reviews. Rheumatology · 2024Review
- Regulation of pain neurotransmitters and chondrocytes metabolism mediated by voltage-gated ion channels: A narrative review.Heliyon · 2023Review
- L-type Voltage-Gated calcium channels partly mediate Mechanotransduction in the intervertebral disc.JOR spine · 2022Article
- Selective block of sensory neuronal T-type/Cav3.2 activity mitigates neuropathic pain behavior in a rat model of osteoarthritis pain.Arthritis research & therapy · 2022Article
- Urocortin-1 Is Chondroprotective in Response to Acute Cartilage Injury via Modulation of Piezo1.International journal of molecular sciences · 2022Article
- Mechanosensory and mechanotransductive processes mediated by ion channels in articular chondrocytes: Potential therapeutic targets for osteoarthritis.Channels (Austin, Tex.) · 2021Review
- Integrins, cadherins and channels in cartilage mechanotransduction: perspectives for future regeneration strategies.Expert reviews in molecular medicine · 2021Review
- The strain-generated electrical potential in cartilaginous tissues: a role for piezoelectricity.Biophysical reviews · 2021Review
- KCells · 2020Review
- Article
- Flow-induced mechanotransduction in skeletal cells.Biophysical reviews · 2019Review
- Spontaneous calcium signaling of cartilage cells: from spatiotemporal features to biophysical modeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Identification of Chondrocyte Genes and Signaling Pathways in Response to Acute Joint Inflammation.Scientific reports · 2019Article
- Physical Stimulations for Bone and Cartilage Regeneration.Regenerative engineering and translational medicine · 2018Article
- Calcium signaling of in situ chondrocytes in articular cartilage under compressive loading: Roles of calcium sources and cell membrane ion channels.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2018Article
- Chondroprotection by urocortin involves blockade of the mechanosensitive ion channel Piezo1.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Voltage-sensitive calcium channels (VSCC) regulate cellular calcium influx, one of the earliest responses to mechanical stimulation in osteoblasts. Here, we postulate that T-type VSCCs play an essential role in bone mechanical response to load and participate in events leading to the pathology of load-induced OA. Repetitive mechanical insult was used to induce OA in Cav3.2 T-VSCC null and wild-type control mouse knees. Osteoblasts (MC3T3-E1) and chondrocytes were treated with a selective T-VSCC inhibitor and subjected to fluid shear stress to determine how blocking of T-VSCCs alters the expression profile of each cell type upon mechanical stimulation. Conditioned-media (CM) obtained from static and sheared MC3T3-E1 was used to assess the effect of osteoblast-derived factors on the chondrocyte phenotype. T-VSCC null knees exhibited significantly lower focal articular cartilage damage than age-matched controls. In vitro inhibition of T-VSCC significantly reduced the expression of both early and late mechanoresponsive genes in osteoblasts but had no effect on gene expression in chondrocytes. Furthermore, treatment of chondrocytes with CM obtained from sheared osteoblasts induced expression of markers of hypertrophy in chondrocytes and this was nearly abolished when osteoblasts were pre-treated with the T-VSCC-specific inhibitor. These results indicate that T-VSCC plays a role in signaling events associated with induction of OA and is essential to the release of osteoblast-derived factors that promote an early OA phenotype in chondrocytes. Further, these findings suggest that local inhibition of T-VSCC may serve as a therapy for blocking load-induced bone formation that results in cartilage degeneration.
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Registered trials
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