June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Molecular coupling between TRPV4 and aquaporin 4 channels mediates osmosensation in Müller glia
Author Affiliations & Notes
  • David Krizaj
    Ophthalmology & Visual Sciences, Univ of Utah School of Med, Salt Lake City, UT
    Physiology, University of Utah School of Med, Salt Lake City, UT
  • Daniel Ryskamp
    Ophthalmology & Visual Sciences, Univ of Utah School of Med, Salt Lake City, UT
  • Andrew Jo
    Ophthalmology & Visual Sciences, Univ of Utah School of Med, Salt Lake City, UT
  • Alan Verkman
    Medicine, University of California San Francisco, San Francisco, CA
  • Nanna Macaulay
    Cellular and Molecular Medicine, University of Copenhagen, Copenhagen, Denmark
  • Footnotes
    Commercial Relationships David Krizaj, None; Daniel Ryskamp, None; Andrew Jo, None; Alan Verkman, None; Nanna Macaulay, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 2673. doi:
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    • Get Citation

      David Krizaj, Daniel Ryskamp, Andrew Jo, Alan Verkman, Nanna Macaulay; Molecular coupling between TRPV4 and aquaporin 4 channels mediates osmosensation in Müller glia. Invest. Ophthalmol. Vis. Sci. 2013;54(15):2673.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: To determine the molecular mechanism of volume regulation in Müller glia, radial astroglia that are central to the control of activity-dependent water fluxes in the vertebrate retina. A combination of biophysical, genetic and physiological approaches was used to characterize reciprocal interactions between the osmosensor TRPV4 and the water channel aquaporin 4 (AQP4) in heterologously expressing Xenopus oocytes, and in Müller glia from wild type and AQP4 knockout mice.

Methods: Cell area, volume and calcium concentration [Ca2+]i were measured under isotonic and hypotonic conditions from wild type and AQP4-/- Müller glia loaded with fluorescent markers of cell volume and intracellular calcium. Transmembrane currents in Xenopus oocytes transfected with combinations of TRPV4, AQP1 and/or AQP4 channels were measured with the two-electrode voltage clamp under isotonic conditions, during mild hypotonic stimulation (HTS) and/or stimulation with selective modulators of TRPV4 function. Stretch-induced currents from outside-out membrane patches were recorded with high-speed pressure clamp.

Results: TRPV4 and AQP4 colocalized in Müller glial endfeet and radial processes. HTS- evoked cation influx and volume increase in Müller cells were sensitive to BAPTA and TRPV4 blockers whereas HTS-induced changes in volume regulation, kinetics of hypotonically induced [Ca2+]i signals, calcium signal amplitudes and the dose-[Ca2+]i response relationship were compromised in mice lacking AQP4. Oocytes co-transfected with TRPV4 and AQP1/AQP4 exhibited a similar rate of swelling (13.0 + 1.5%/100 sec vs. 14.1+1.3%/100 sec), however, HTS facilitated cation fluxes in TRPV4-expressing cells that co-expressed AQP4, but not AQP1. This effect was sensitive to TRPV4 antagonists, indicating that it was mediated through TRPV4 channels. Consistent with this, TRPV4 agonist-induced Ca entry into transfected oocytes was augmented by the presence of AQP4.

Conclusions: Our data suggest that a macromolecular complex consisting of a stretch sensor and a water channel (TRPV4 and AQP4) regulates osmotically-induced cation fluxes in Müller glia. The complex senses and responds to changes in osmolarity, rather than changes in cell volume. TRPV4-AQP4 channels are strategically localized to Müller endfeet where they may regulate retina:blood fluxes driven by the metabolism, intraocular pressure and retinal pathologies.

Keywords: 603 Muller cells • 691 retina: proximal (bipolar, amacrine, and ganglion cells) • 505 edema  
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