ArticleJournal of muscle research and cell motility2002
Role of K+ channels in L-6 myoblast migration.
Article in Journal of muscle research and cell motility, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed, 5 citations in OpenAlex.
- Enhancing Human Cutaneous Wound Healing through Targeted Suppression of Large Conductance CaInternational journal of molecular sciences · 2024Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Migration of myoblasts is an important component of the reparative response to muscle injury, and furthermore may be a key determinant of the success of myoblast transplantation for the treatment of genetic muscle diseases. The present study examined the hypothesis that K+ channels modulate myoblast migration. The migration of cultured L-6 myoblasts was assessed in vitro on confluent cultures with the razor wound method, in the absence and presence of the following agents: 3,4-diaminopyridine and tetraethylammonium (which block several types of K+ channels), apamin and charybdotoxin (which block Ca++-activated K+ channels), glibenclamide (which blocks ATP-sensitive K+ channels), and alpha-, beta-, gamma-, and delta-dendrotoxin (which block voltage-gated K+ channels). Migration was assessed with respect to number of migrated cells, average distance migrated, and total distance migrated. Overall, myoblast migration was stimulated in response to low concentrations of tetraethylammonium, apamin, glibenclamide, and alpha-, beta- and delta-dendrotoxin. With these agents, the number of migrated cells increased by 28-47%, the average distance migrated increased by 22-35%, and the total distance migrated increased by 60-85%. Conversely, migration was inhibited by high concentrations of 3,4-diaminopyridine, tetraethylammonium, and all dendrotoxins. These data indicate that in L-6 myoblasts migration is regulated by K+ channels, and that several types of K+ channels appear to participate in cell migration.
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Registered trials
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