ArticleInvestigative ophthalmology & visual science2020
Signaling Between TRPV1/TRPV4 and Intracellular Hydrostatic Pressure in the Mouse Lens.
Article in Investigative ophthalmology & visual science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 31 citations in OpenAlex.
- CatExperimental eye research · 2026Article
- Extrinsic Modulation of the Zonular Tension Induces Calcium Influx in Lens Fiber Cells That Is Mediated by Mechanosensitive TRPV1 and TRPV4 Channels.Investigative ophthalmology & visual science · 2026Article
- Lens Biomechanics and Mechanotransduction Signaling: Dual Pillars of Age-Related Cataract Pathogenesis.Investigative ophthalmology & visual science · 2026Review
- Regional Differences in Calcium Dynamics in the Intact Lens: The Role of TRPV Channels in Lens Calcium Regulation.Investigative ophthalmology & visual science · 2025Article
- Studies on Hydrostatic Pressure Responses to Piezo1 and TRPV4 in the Mouse Lens.Investigative ophthalmology & visual science · 2025Article
- The Collapse of Brain Clearance: Glymphatic-Venous Failure, Aquaporin-4 Breakdown, and AI-Empowered Precision Neurotherapeutics in Intracranial Hypertension.International journal of molecular sciences · 2025Review
- Transient Receptor Potential Channels in Physiology and Pathophysiology: Special Issue.International journal of molecular sciences · 2025Article
- Combinatorial genetic manipulation of Cx50, PI3K and PTEN alters postnatal mouse lens growth and homeostasis.Frontiers in ophthalmology · 2025Article
- TRPV1-dependent NKCC1 activation in mouse lens involves integrin and the tubulin cytoskeleton.Journal of cellular physiology · 2024Article
- Minimizing Oxidative Stress in the Lens: Alternative Measures for Elevating Glutathione in the Lens to Protect against Cataract.Antioxidants (Basel, Switzerland) · 2024Review
- Effect of hydrogen peroxide on lens transparency, intracellular pH, gap junction coupling, hydrostatic pressure and membrane water permeability.Experimental eye research · 2024Article
- Connexin 50 Influences the Physiological Optics of the In Vivo Mouse Lens.Investigative ophthalmology & visual science · 2024Article
- Verification of the gene and protein expression of the aquaglyceroporin AQP3 in the mammalian lens.Experimental eye research · 2024Article
- The significance of growth shells in development of symmetry, transparency, and refraction of the human lens.Frontiers in ophthalmology · 2024Review
- Modulation of Membrane Trafficking of AQP5 in the Lens in Response to Changes in Zonular Tension Is Mediated by the Mechanosensitive Channel TRPV1.International journal of molecular sciences · 2023Article
- Mechanical Stretch Activates TRPV4 and Hemichannel Responses in the Nonpigmented Ciliary Epithelium.International journal of molecular sciences · 2023Article
- Patch clamp studies on TRPV4-dependent hemichannel activation in lens epithelium.Frontiers in pharmacology · 2023Article
- Insights into the biochemical and biophysical mechanisms mediating the longevity of the transparent optics of the eye lens.The Journal of biological chemistry · 2022Review
- Activation of Piezo1 Increases Na,K-ATPase-Mediated Ion Transport in Mouse Lens.International journal of molecular sciences · 2022Article
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Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Purpose: The lens uses feedback to maintain zero pressure in its surface cells. Positive pressures are detected by transient receptor potential vanilloid (TRPV4), which initiates a cascade that reduces surface cell osmolarity. The first step is opening of gap junction hemichannels. One purpose of the current study was to identify the connexin(s) in the hemichannels. Negative pressures are detected by TRPV1, which initiates a cascade that increases surface osmolarity. The increase in osmolarity was initially reported to be through inhibition of Na/K ATPase activity, but a recent study reported it was through stimulation of Na/K/2Cl (NKCC) cotransport. A second purpose of this study was to reconcile these two reports. Methods: Intracellular hydrostatic pressures were measured using a microelectrode/manometer system. Lenses from TRPV1 or Cx50 null mice were studied. Specific inhibitors of Cx50 gap junction channels, NKCC, and Akt were used. Results: Either knockout of Cx50 or blockade of Cx50 channels completely eliminated the response to positive surface pressures. Knockout of Cx50 also caused a positive drift in surface pressure. The short-term (∼20-minute) response to negative surface pressures was eliminated by blockade of NKCC, but a long-term (∼4-hour) response restored pressure to zero. Both short- and long-term responses were eliminated by knockout of TRPV1 or inhibition of Akt. Conclusions: Hemichannels made from Cx50 are required for the response to positive surface pressures. Negative surface pressures first activate NKCC, but a backup system is inhibition of Na/K ATPase activity. Both responses are initiated by TRPV1 and go through PI3K/Akt before branching.
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Registered trials
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.