ArticleJournal of muscle research and cell motility1998
Involvement of the cytoskeleton in calcium-dependent stress relaxation of rat aortic smooth muscle.
Article in Journal of muscle research and cell motility, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Loss of smooth muscle α-actin effects on mechanosensing and cell-matrix adhesions.Experimental biology and medicine (Maywood, N.J.) · 2020Article
- Ca2+-dependent actin remodeling in the contracting A7r5 cell.Journal of muscle research and cell motility · 2001Article
- Remodeling of the actin cytoskeleton in the contracting A7r5 smooth muscle cell.Journal of muscle research and cell motility · 2000Article
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
Rat aortic smooth muscle exhibits a remarkable capacity for stress relaxation, the release of tension following tissue stretch. Stress relaxation was markedly enhanced in contracted aortic rings compared with unstimulated tissue. The magnitude of stress relaxation in contracted aortic rings correlated well with the passive tension imposed on the tissue by stretching, but showed little relationship to changes in tissue length or to the level of tension developed in response to agonist stimulation prior to stretch. The enhancement of stress relaxation in precontracted tissue was not affected by intimal rubbing or treatment with L-NAME. By comparison, the removal of extracellular calcium markedly attenuated stress relaxation. In addition, the use of cytochalasin B to block actin polymerization inhibited stress relaxation, whereas colchicine, a drug used to cause microtubule disassembly, had no effect on the phenomenon. The results indicate that the enhanced stress relaxation in contracted tissue is a calcium-dependent process and is not due to passive tissue elastic properties. We suggest that stress relaxation may not involve cross-bridge formation but could be explained by the remodelling of a portion of the tension-bearing actin cytoskeleton.
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Registered trials
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