TRPV4 channel activation selectively inhibits tumor endothelial cell proliferation
Open accessAbstract
Endothelial cell proliferation is a critical event during angiogenesis, regulated by both soluble factors and mechanical forces. Although the proliferation of tumor cells is studied extensively, little is known about the proliferation of tumor endothelial cells (TEC) and its contribution to tumor angiogenesis. We have recently shown that reduced expression of the mechanosensitive ion channel TRPV4 in TEC causes aberrant mechanosensitivity that result in abnormal angiogenesis. Here, we show that TEC display increased proliferation compared to normal endothelial cells (NEC). Further, we found that TEC exhibit high basal ERK1/2 phosphorylation and increased expression of proliferative genes important in the G1/S phase of the cell cycle. Importantly, pharmacological activation of TRPV4, with a small molecular activator GSK1016790A (GSK), significantly inhibited TEC proliferation, but had no effect on the proliferation of NEC or the tumor cells (epithelial) themselves. This reduction in TEC proliferation by TRPV4 activation was correlated with a decrease in high basal ERK1/2 phosphorylation. Finally, using a syngeneic tumor model revealed that TRPV4 activation, with GSK, significantly reduced endothelial cell proliferation in vivo. Our findings suggest that TRPV4 channels regulate tumor angiogenesis by selectively inhibiting tumor endothelial cell proliferation.
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Using simple, direct modulation of TRPV4 with GSK101 in a 3D microfluidic system, vascular integrity can be tuned to recapitulate known TRPV4 physiological functions in vivo, especially in pulmonary edema, and achieve vascular leakiness comparable with previous MTM studies using tumor cells.
“Using this simple, direct modulation of TRPV4 with GSK101 in a 3D micro fl uidic system, we can therefore tune the vascular integrity to recapitulate known TRPV4 physiological functions in vivo, especially in pulmonary edema, 28,30,51,52 and achieve vascular leakiness in a manner that is comparable with previous MTM studies using tumor cells. 2,53”
From Rapid Assessment of Nanoparticle Extravasation in a Microfluidic Tumor Model (2019) · cites this paper as [51]
The Discussion (page unavailable) reports that GSK activation of TRPV4 normalizes tumor vasculature, supporting the cited comparison to tumor-vessel studies in general. It does not report vascular leakiness or establish that the degree of leakiness is comparable to the citing study’s 3D microfluidic system. The pulmonary-edema portion is attached to other citations. (LLM, conf=0.82)
Experimental — accuracy not yet measuredHUVECs may not entirely recapitulate all known roles for TRPV4 in tumor vasculature.
“HUVECs may not entirely recapitulate all known roles for TRPV4 in tumor vasculature. 24,28,35,51,53,66”
From Rapid Assessment of Nanoparticle Extravasation in a Microfluidic Tumor Model (2019) · cites this paper as [51]
The Results (page unavailable) report that tumor endothelial cells proliferated more than normal endothelial cells and that TRPV4 activation did not affect normal endothelial-cell proliferation. This supports the caution that normal endothelial cells may not capture TRPV4's roles in tumor vasculature, but the study did not examine HUVECs specifically or establish the full range of those roles. (LLM, conf=0.83)
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Mechanosensitive TRPV4 Trafficking Drives TGF-Β-Mediated Mesenchymal Transition in Colorectal Cancer
Karaca, C., & Başbınar, Y. (2025) · Journal of Basic and Clinical Health Sciences · doi:10.30621/jbachs.1606073
BindingDB Entry 50011116: Recent advances in TRPV4 agonists and antagonists.
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- Authors
- Thoppil, R. J., Adapala, R. K., Cappelli, H. C., Kondeti, V., Dudley, A. C., Gary Meszaros, J., Paruchuri, S., & Thodeti, C. K.
- Affiliations
- Kent State University (US)
- University of Akron (US)
- University of North Carolina at Chapel Hill (US)
- Corresponding author
- Thodeti, Charles K.
- Venue
- Scientific Reports
- Published
- 2015-09-21
- Volume
- 5
- Issue
- 1
- Pages
- 14257-14257
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC4585691
- OpenAlex
- W2328403892
- Cited by
- 63
- References
- 30
- Citations by year
- 2025: 4 · 2024: 8 · 2023: 4 · 2022: 7 · 2021: 9 · 2020: 7 · 2019: 10 · 2018: 7 · 2017: 5 · 2016: 2
- FWCI
- 2.03
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- UNC Libraries
- Funders
- American Heart Association (14GRNT20380935)
- Northeast Ohio Medical University
- National Cancer Institute (R01CA177875)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Keywords
- TRPV4, tumor endothelial cells, endothelial cell proliferation, tumor angiogenesis, mechanosensitive ion channels, ERK1/2 phosphorylation, GSK1016790A, G1/S cell cycle, syngeneic mouse model
- MeSH terms
- Animals, Antineoplastic Agents, Leucine, Neoplasms, Neovascularization, Pathologic, Sulfonamides, Up-Regulation, MAP Kinase Signaling System, Endothelial Cells, Cell Proliferation, TRPV Cation Channels, Mice
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