ArticleBone2016
T-Type voltage-sensitive calcium channels mediate mechanically-induced intracellular calcium oscillations in osteocytes by regulating endoplasmic reticulum calcium dynamics.
Article in Bone, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Real-Time Axial Motion Compensation for Intravital Two-Photon Imaging of Mechanically Loaded Bone.bioRxiv : the preprint server for biology · 2026Article
- Impacts of Nonenzymatic Glycation Crosslinks in Bone Matrix on the Mechanosensitivity of Osteocyte.Calcified tissue international · 2025Article
- Loss of the auxiliary αJBMR plus · 2024Article
- Transient plasma membrane disruption induced calcium waves in mouse and human corneal epithelial cells.PloS one · 2024Article
- Examining Mechanisms for Voltage-Sensitive Calcium Channel-Mediated Secretion Events in Bone Cells.Calcified tissue international · 2023Review
- Gabapentin Disrupts Binding of Perlecan to the αBiomolecules · 2022Article
- Mechanosensitive piezo1 calcium channel activates connexin 43 hemichannels through PI3K signaling pathway in bone.Cell & bioscience · 2022Article
- Effects of Gabapentin and Pregabalin on Calcium Homeostasis: Implications for Physical Rehabilitation of Musculoskeletal Tissues.Current osteoporosis reports · 2022Review
- The Diminishing Returns of Mechanical Loading and Potential Mechanisms that Desensitize Osteocytes.Current osteoporosis reports · 2021Review
- Review
- Osteocyte mechanosensing following short-term and long-term treatment with sclerostin antibody.Bone · 2021Article
- Skeletal Functions of Voltage Sensitive Calcium Channels.Current osteoporosis reports · 2021Review
- Targeting Mechanotransduction in Osteosarcoma: A Comparative Oncology Perspective.International journal of molecular sciences · 2020Review
- Article
- CACNA1H downregulation induces skeletal muscle atrophy involving endoplasmic reticulum stress activation and autophagy flux blockade.Cell death & disease · 2020Article
- miR-137 and its target T-type CaCell proliferation · 2020Article
- Transient Cell Membrane Disruptions induce Calcium Waves in Corneal Keratocytes.Scientific reports · 2020Article
- Osteocyte-Mediated Translation of Mechanical Stimuli to Cellular Signaling and Its Role in Bone and Non-bone-Related Clinical Complications.Current osteoporosis reports · 2020Review
- Article
- Genetic T-type calcium channelopathies.Journal of medical genetics · 2020Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
One of the earliest responses of bone cells to mechanical stimuli is a rise in intracellular calcium (Ca(2+)), and osteocytes in particular exhibit robust oscillations in Ca(2+) when subjected to loading. Previous studies implicate roles for both the endoplasmic reticulum (ER) and T-Type voltage-sensitive calcium channels (VSCC) in these responses, but their interactions or relative contributions have not been studied. By observing Ca(2+) dynamics in the cytosol (Ca(2+)cyt) and the ER (Ca(2+)ER), the focus of this study was to explore the role of the ER and T-Type channels in Ca(2+) signaling in bone cells. We demonstrate that inhibition of T-Type VSCC in osteocytes significantly reduces the number of Ca(2+)cyt responses and affects Ca(2+)ER depletion dynamics. Simultaneous observation of Ca(2+) exchange among these spaces revealed high synchrony between rises in Ca(2+)cyt and depressions in Ca(2+)ER, and this synchrony was significantly reduced by challenging T-Type VSCC. We further confirmed that this effect was mediated directly through the ER and not through store-operated Ca(2+) entry (SOCE) pathways. Taken together, our data suggests that T-Type VSCC facilitate the recovery of Ca(2+)ER in osteocytes to sustain mechanically-induced Ca(2+) oscillations, uncovering a new mechanism underlying the behavior of osteocytes as mechanosensors.
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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.