ArticleJournal of biomedical science2010
Caldesmon regulates the motility of vascular smooth muscle cells by modulating the actin cytoskeleton stability.
Article in Journal of biomedical science, 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, 32 citations in OpenAlex.
- Caldesmon-1-mediated actin dynamics is essential for osteogenic differentiation of aortic valve interstitial cells.Scientific reports · 2026Article
- Emerging role of caldesmon in cancer: A potential biomarker for colorectal cancer and other cancers.World journal of gastrointestinal oncology · 2022Review
- Caldesmon ablation in mice causes umbilical herniation and alters contractility of fetal urinary bladder smooth muscle.The Journal of general physiology · 2021Article
- Single-Cell Transcriptome Analysis of Human Adipose-Derived Stromal Cells Identifies a Contractile Cell Subpopulation.Stem cells international · 2021Article
- L-caldesmon alters cell spreading and adhesion force in RANKL-induced osteoclasts.Journal of biomedical science · 2019Article
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- DL0805-2, a novel indazole derivative, relaxes angiotensin II-induced contractions of rat aortic rings by inhibiting Rho kinase and calcium fluxes.Acta pharmacologica Sinica · 2016Article
- Article
- Article
- Genetics of cerebral vasospasm.Neurology research international · 2013Article
- The conformational state of actin filaments regulates branching by actin-related protein 2/3 (Arp2/3) complex.The Journal of biological chemistry · 2012Article
- Modulating the dysregulated migration of pulmonary arterial hypertensive smooth muscle cells with motif mimicking cell permeable peptides.Current topics in peptide & protein researchArticle
- Diversification of caldesmon-linked actin cytoskeleton in cell motility.Cell adhesion & migrationReview
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundMigration of vascular smooth muscle cells (SMCs) from the media to intima constitutes a critical step in the development of proliferative vascular diseases. To elucidate the regulatory mechanism of vacular SMC motility, the roles of caldesmon (CaD) and its phosphorylation were investigated.
methodsWe have performed Transwell migration assays, immunofluorescence microscopy, traction microscopy and cell rounding assays using A7r5 cells transfected with EGFP (control), EGFP-wtCaD or phosphomimetic CaD mutants, including EGFP-A1A2 (the two PAK sites Ser452 and Ser482 converted to Ala), EGFP-A3A4 (the two Erk sites Ser497 and Ser527 converted to Ala), EGFP-A1234 (both PAK- and Erk-sites converted to Ala) and EGFP-D1234 (both PAK- and Erk-sites converted to Asp).
resultsWe found that cells transfected with wtCaD, A1A2 or A3A4 mutants of CaD migrated at a rate approximately 50% more slowly than those EGFP-transfected cells. The migration activity for A1234 cells was only about 13% of control cells. Thus it seems both MAPK and PAK contribute to the motility of A7r5 cells and the effects are comparable and additive. The A1234 mutant also gave rise to highest strain energy and lowest rate of cell rounding. The migratory and contractile properties of these cells are consistent with stabilized actin cytoskeletal structures. Indeed, the A1234 mutant cells exhibited most robust stress fibers, whereas cells transfected with wtCaD or A3A4 (and A1A2) had moderately reinforced actin cytoskeleton. The control cells (transfected with EGFP alone) exhibited actin cytoskeleton that was similar to that in untransfected cells, and also migrated at about the same speed as the untransfected cells.
conclusionsThese results suggest that both the expression level and the level of MAPK- and/or PAK-mediated phosphorylation of CaD play key roles in regulating the cell motility by modulating the actin cytoskeleton stability in dedifferentiated vascular SMCs such as A7r5.
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