ArticleJournal of bone and mineral metabolism2011
L-type calcium channel activity in osteoblast cells is regulated by the actin cytoskeleton independent of protein trafficking.
Article in Journal of bone and mineral metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed, 18 citations in OpenAlex.
- Selective adhesion inhibition and hyaluronan envelope reduction of dermal tumor cells by cold plasma-activated medium.Cell adhesion & migration · 2023Article
- The Mechanotransduction Signaling Pathways in the Regulation of Osteogenesis.International journal of molecular sciences · 2023Review
- Primary human chondrocytes respond to compression with phosphoproteomic signatures that include microtubule activation.Journal of biomechanics · 2019Article
- Fluid flow facilitates inward rectifier KScientific reports · 2016Article
- 5α-Dihydrotestosterone regulates the expression of L-type calcium channels and calcium-binding protein regucalcin in human breast cancer cells with suppression of cell growth.Medical oncology (Northwood, London, England) · 2015Article
- Forskolin Regulates L-Type Calcium Channel through Interaction between Actinin 4 and β3 Subunit in Osteoblasts.PloS one · 2015Article
- Evaluating the electrical stimulation of bone cells based on an induced transmembrane potential model and intracellular calcium levels.Journal of tissue engineeringArticle
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Voltage-dependent L-type calcium channels (VDCC) play important roles in many cellular processes. The interaction of the actin cytoskeleton with the channel in nonexcitable cells is less well understood. We performed whole-cell patch-clamp surface biotinylation and calcium imaging on different osteoblast cells to determine channel kinetics, amplitude, surface abundance, and intracellular calcium, respectively. Patch-clamp studies showed that actin polymerization by phalloidin increased the peak current density of I (Ca), whereas actin depolymerization by cytochalasin D (CD) significantly decreased the current amplitude. This result is consistent with calcium imaging, which showed that CD significantly decreased Bay K8644-induced intracellular calcium increase. Surface biotinylation studies showed that CD is not able to affect the surface expression of the pore-forming subunit α(1C). Interestingly, application of CD caused a significantly negative shift in the steady-state inactivation kinetics of I (Ca). There were decreases in the voltage at half-maximal inactivation that changed in a dose-dependent manner. CD also reduced the effect of activated vitamin D(3) (1α,25-D3) on VDCC and intracellular calcium. We conclude that in osteoblasts the actin cytoskeleton affects α(1C) by altering the channel kinetic properties, instead of changing the surface expression, and it is able to regulate 1α,25-D3 signaling through VDCC. Our study provides a new insight into calcium regulation in osteoblasts, which are essential in many physiological functions of this cell.
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Registered trials
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