ArticlePflugers Archiv : European journal of physiology2015
TRPV4 participates in the establishment of trailing adhesions and directional persistence of migrating cells.
Article in Pflugers Archiv : European journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Coordinated in confined migration: crosstalk between the nucleus and ion channel-mediated mechanosensation.Trends in cell biology · 2024Review
- Article
- TRPV4 Stimulation Level Regulates CaMembranes · 2022Article
- The interplay between physical cues and mechanosensitive ion channels in cancer metastasis.Frontiers in cell and developmental biology · 2022Review
- Protein Kinase A in cellular migration-Niche signaling of a ubiquitous kinase.Frontiers in molecular biosciences · 2022Review
- TRPV Protein Family-From Mechanosensing to Cancer Invasion.Biomolecules · 2021Review
- Mechanosensitive ion channels in cell migration.Cells & development · 2021Review
- Thermosensitive TRPV4 channels mediate temperature-dependent microglia movement.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Neuropathy-causing TRPV4 mutations disrupt TRPV4-RhoA interactions and impair neurite extension.Nature communications · 2021Article
- Cross-talk between the calcium channel TRPV4 and reactive oxygen species interlocks adhesive and degradative functions of invadosomes.The Journal of cell biology · 2021Article
- TRP Channels and Small GTPases Interplay in the Main Hallmarks of Metastatic Cancer.Frontiers in pharmacology · 2020Review
- Protonation of Piezo1 Impairs Cell-Matrix Interactions of Pancreatic Stellate Cells.Frontiers in physiology · 2020Article
- Transient receptor potential ion-channel subfamily V member 4: a potential target for cancer treatment.Cell death & disease · 2019Review
- TRPV4-mediated calcium signaling in mesenchymal stem cells regulates aligned collagen matrix formation and vinculin tension.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- A TR(i)P to Cell Migration: New Roles of TRP Channels in Mechanotransduction and Cancer.Frontiers in physiology · 2019Review
- The Role of TRP Channels in the Metastatic Cascade.Pharmaceuticals (Basel, Switzerland) · 2018Review
- Piezo2 channel regulates RhoA and actin cytoskeleton to promote cell mechanobiological responses.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Basal cells express functional TRPV4 channels in the mouse nasal epithelium.Biochemistry and biophysics reports · 2015Article
- Novel mutations highlight the key role of the ankyrin repeat domain in TRPV4-mediated neuropathy.Neurology. Genetics · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcium signaling participates in different cellular processes leading to cell migration. TRPV4, a non-selective cation channel that responds to mechano-osmotic stimulation and heat, is also involved in cell migration. However, the mechanistic involvement of TRPV4 in cell migration is currently unknown. We now report that expression of the mutant channel TRPV4-(121)AAWAA (lacking the phosphoinositide-binding site (121)KRWRK(125) and the response to physiological stimuli) altered HEK293 cell migration. Altered migration patterns included periods of fast and persistent motion followed by periods of stalling and turning, and the extension of multiple long cellular protrusions. TRPV4-WT overexpressing cells showed almost complete loss of directionality with frequent turns, no progression, and absence of long protrusions. Traction microscopy revealed higher tractions forces in the tail of TRPV4-(121)AAWAA than in TRPV4-WT expressing cells. These results are consistent with a defective and augmented tail retraction in TRPV4-(121)AAWAA- and TRPV4-WT-expressing cells, respectively. The activity of calpain, a protease implicated in focal adhesion (FA) disassembly, was decreased in TRPV4-(121)AAWAA compared with TRPV4-WT-expressing cells. Consistently, larger focal adhesions were seen in TRPV4-(121)AAWAA compared with TRPV4-WT-expressing HEK293 cells, a result that was also reproduced in T47D and U87 cells. Similarly, overexpression of the pore-dead mutant TRPV4-M680D resumed the TRPV4-(121)AAWAA phenotype presenting larger FA. The migratory phenotype obtained in HEK293 cells overexpressing TRPV4-(121)AAWAA was mimicked by knocking-down TRPC1, a cationic channel that participates in cell migration. Together, our results point to the participation of TRPV4 in the dynamics of trailing adhesions, a function that may require the interplay of TRPV4 with other cation channels or proteins present at the FA sites.
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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.