ArticleExperimental & molecular medicine2010
TRPC3 cation channel plays an important role in proliferation and differentiation of skeletal muscle myoblasts.
Article in Experimental & molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Ion Channels and Transporters in Muscle Cell Differentiation.International journal of molecular sciences · 2021Review
- TRPCs: Influential Mediators in Skeletal Muscle.Cells · 2020Review
- The LRRC8/VRAC anion channel facilitates myogenic differentiation of murine myoblasts by promoting membrane hyperpolarization.The Journal of biological chemistry · 2019Article
- TRPC channels in exercise-mimetic therapy.Pflugers Archiv : European journal of physiology · 2019Review
- With the greatest care, stromal interaction molecule (STIM) proteins verify what skeletal muscle is doing.BMB reports · 2018Review
- A focus on extracellular CaExperimental & molecular medicine · 2017Review
- Mitsugumin 53 regulates extracellular CaScientific reports · 2016Article
- Increased expression of transient receptor potential canonical 6 (TRPC6) in differentiating human megakaryocytes.Cell biology international · 2016Article
- Interaction between mitsugumin 29 and TRPC3 participates in regulating Ca(2+) transients in skeletal muscle.Biochemical and biophysical research communications · 2015Article
- Transient Receptor Potential Canonical 1 (TRPC1) Channels as Regulators of Sphingolipid and VEGF Receptor Expression: IMPLICATIONS FOR THYROID CANCER CELL MIGRATION AND PROLIFERATION.The Journal of biological chemistry · 2015Article
- Store-operated Ca2+ entry in muscle physiology and diseases.BMB reports · 2014Review
- Pdx-1 activates islet α- and β-cell proliferation via a mechanism regulated by transient receptor potential cation channels 3 and 6 and extracellular signal-regulated kinases 1 and 2.Molecular and cellular biology · 2013Article
- The CHC22 clathrin-GLUT4 transport pathway contributes to skeletal muscle regeneration.PloS one · 2013Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During membrane depolarization associated with skeletal excitation-contraction (EC) coupling, dihydropyridine receptor [DHPR, a L-type Ca(2+) channel in the transverse (t)-tubule membrane] undergoes conformational changes that are transmitted to ryanodine receptor 1 [RyR1, an internal Ca(2+)-release channel in the sarcoplasmic reticulum (SR) membrane] causing Ca(2+) release from the SR. Canonical-type transient receptor potential cation channel 3 (TRPC3), an extracellular Ca(2+)-entry channel in the t-tubule and plasma membrane, is required for full-gain of skeletal EC coupling. To examine additional role(s) for TRPC3 in skeletal muscle other than mediation of EC coupling, in the present study, we created a stable myoblast line with reduced TRPC3 expression and without alpha1((S))DHPR (MDG/TRPC3 KD myoblast) by knock-down of TRPC3 in alpha1((S))DHPR-null muscular dysgenic (MDG) myoblasts using retrovirus-delivered small interference RNAs in order to eliminate any DHPR-associated EC coupling-related events. Unlike wild-type or alpha1((S))DHPR-null MDG myoblasts, MDG/TRPC3 KD myoblasts exhibited dramatic changes in cellular morphology (e.g., unusual expansion of both cell volume and the plasma membrane, and multi-nuclei) and failed to differentiate into myotubes possibly due to increased Ca(2+) content in the SR. These results suggest that TRPC3 plays an important role in the maintenance of skeletal muscle myoblasts and myotubes.
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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.