ArticleBritish journal of pharmacology2014
TRPC6 regulates cell cycle progression by modulating membrane potential in bone marrow stromal cells.
Article in British journal of pharmacology, 2014. 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, 23 citations in OpenAlex.
- TRPC6-Mediated CaCells · 2026Article
- Review
- Mechanosensitive cation currents through TRPC6 and Piezo1 channels in human pulmonary arterial endothelial cells.American journal of physiology. Cell physiology · 2022Article
- New Insights into TRP Ion Channels in Stem Cells.International journal of molecular sciences · 2022Review
- Mechanosensitive channel Piezo1 is required for pulmonary artery smooth muscle cell proliferation.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- TRPC6, a therapeutic target for pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Sevoflurane preconditioning promotes mesenchymal stem cells to relieve myocardial ischemia/reperfusion injury via TRPC6-induced angiogenesis.Stem cell research & therapy · 2021Article
- Trpc1 as the Missing Link Between the Bmp and CaScientific reports · 2019Article
- TRPC6 regulates phenotypic switching of vascular smooth muscle cells through plasma membrane potential-dependent coupling with PTEN.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- TRPC1 intensifies house dust mite-induced airway remodeling by facilitating epithelial-to-mesenchymal transition and STAT3/NF-κB signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- TRPC6 in simulated microgravity of intervertebral disc cells.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2018Article
- Transient receptor potential vanilloid-3 (TRPV3) activation plays a central role in cardiac fibrosis induced by pressure overload in rats via TGF-βNaunyn-Schmiedeberg's archives of pharmacology · 2018Article
- Role of transient receptor potential channel 6 in the odontogenic differentiation of human dental pulp cells.Experimental and therapeutic medicine · 2017Article
- Bioelectrical regulation of cell cycle and the planarian model system.Biochimica et biophysica acta · 2015Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeCa(2+) influx is important for cell cycle progression, but the mechanisms involved seem to vary. We investigated the potential roles of transient receptor potential (TRP) channels and store-operated Ca(2+) entry (SOCE)-related molecules STIM (stromal interaction molecule)/Orai in the cell cycle progression of rat bone marrow stromal cells (BMSCs), a reliable therapeutic resource for regenerative medicine. EXPERIMENTAL APPROACH: PCR and immunoblot analyses were used to examine mRNA and protein levels, fluorescence imaging and patch clamping for Ca(2+) influx and membrane potential measurements, and flow cytometry for cell cycle analysis. KEY
resultsCell cycle synchronization of BMSCs revealed S phase-specific enhancement of TRPC1, STIM and Orai mRNA and protein expression. In contrast, TRPC6 expression decreased in the S phase and increased in the G1 phase. Resting membrane potential (RMP) of BMSCs was most negative and positive in the S and G1 phases, respectively, and was accompanied by an enhancement and attenuation of SOCE respectively. Chemically depolarizing/hyperpolarizing the membrane erased these differences in SOCE magnitude during the cell cycle. siRNA knockdown of TRPC6 produced a negative shift in RMP, increased SOCE and caused redistribution of BMSCs with increased populations in the S and G2 /M phases and accumulation of cyclins A2 and B1. A low concentration of Gd(3+) (1 μM) suppressed BMSC proliferation at its concentration to inhibit SOC channels relatively specifically. CONCLUSIONS AND IMPLICATIONS: TRPC6, by changing the membrane potential, plays a pivotal role in controlling the SOCE magnitude, which is critical for cell cycle progression of BMSCs. This finding provides a new therapeutic strategy for regulating BMSC proliferation.
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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.