Cell Membrane Stretch Modulates the High-Conductance Ca<sup>2+</sup>-Activated K<sup>+</sup>Channel in Bovine Trabecular Meshwork Cells

Gasull, Xavier; Ferrer, Elisa; Llobet, Artur; Castellano, Antonio; Nicolás, José M.; Palés, Jorge; Gual, Arcadi

doi:10.1167/iovs.02-0384

Cited by 55 publications

(48 citation statements)

References 38 publications

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“…The SAKCaC activation occurred in the absence of intracellular Ca 2+ , suggesting that membrane stretch directly activated the channel. All these results are in agreement with those reported previously [9,23,28].…”

Section: Activation Of Sakcac By Membrane Stretchsupporting

confidence: 94%

“…These channels transduce mechanical stimuli into intracellular signals, such as elevation in intracellular Ca 2+ concentration and electrical activities [1][2][3][4][5][6], which are important in many physiological functions and pathological conditions, for example, sound detection [4], cell volume regulation [7], touch sensation [8], hypo-osmotic shock protection [9], cell locomotion [10], muscular dystrophy and cardiac arrhythmias [11]. The BK channel is one type of MS channels which is widely expressed in both excitable and non-excitable cells and plays an important role in, for example, vascular smooth muscle tone regulation, neuronal firing and endocrine cell secretion [12][13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

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Tuning the mechanosensitivity of a BK channel by changing the linker length

Zhao

Sokabe

2008

Cell Res

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Some large-conductance Ca 2+ and voltage-activated K + (BK) channels are activated by membrane stretch. However, the mechanism of mechano-gating of the BK channels is still not well understood. Previous studies have led to the proposal that the linker-gating ring complex functions as a passive spring, transducing the force generated by intracellular Ca 2+ to the gate to open the channel. This raises the question as to whether membrane stretch is also transmitted to the gate of mechanosensitive (MS) BK channels via the linker-gating complex. To study this, we changed the linker length in the stretch-activated BK channel (SAKCaC), and examined the effect of membrane stretch on the gating of the resultant mutant channels. Shortening the linker increased, whereas extending the linker reduced, the channel mechanosensitivity both in the presence and in the absence of intracellular Ca 2+ . However, the voltage and Ca 2+ sensitivities were not significantly altered by membrane stretch. Furthermore, the SAKCaC became less sensitive to membrane stretch at relatively high intracellular Ca 2+ concentrations or membrane depolarization. These observations suggest that once the channel is in the open-state conformation, tension on the spring is partially released and membrane stretch is less effective. Our results are consistent with the idea that membrane stretch is transferred to the gate via the linker-gating ring complex of the MS BK channels.

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Section: Activation Of Sakcac By Membrane Stretchsupporting

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Tuning the mechanosensitivity of a BK channel by changing the linker length

Zhao

Sokabe

2008

Cell Res

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“…The K + -channel blocker TEA, applied at 7.5 mM during the course of 28 experiments, reduced whole cell currents at +80 mV by 59 ±3% (P<0.001). The response to TEA was consistent with previous observations that K + channels provide a large fraction of the total TM-cell membrane conductance (Fleischhauer et al, 2003;Gasull et al, 2003;Stumpff et al, 1997). …”

Section: Whole-cell Currentssupporting

confidence: 91%

Cell-specific differential modulation of human trabecular meshwork cells by selective adenosine receptor agonists

Karl

Peterson-Yantorno

Civan

2007

Experimental Eye Research

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Activation of A 1 and A 2A subtype adenosine receptors (AR) likely exert opposing effects on outflow of aqueous humor, and thereby, on intraocular pressure. Selective agonists of adenosine receptor (AR) subtypes have previously been applied to trabecular meshwork (TM) and Schlemm's canal (SC) cells to identify the site(s) of differential purinergic modulation. However, the apparent changes in volume monitored by previously measuring projected cell area might have partially reflected cell contraction and relaxation. In addition, whole-cell current responses of the TM cells previously described were highly variable following application of selective A 1 , A 2A and A 3 agonists. The complexity of the electrophysiologic responses may have reflected cell heterogeneity of the populations harvested from collagenase digestion of TM explants. We now report measurements of TM-cell volume using calcein fluorescence quenching, an approach independent of contractile state. Furthermore, we have applied selective AR agonists to a uniform population of human TM cells, the hTM5 cell line. A 1 , but not A 2A or A 3 , AR agonists triggered TM-cell shrinkage. Both A 1 and A 2A AR agonists produced reproducible increases in TM-cell whole-cell currents of similar magnitude.The results suggest that previous measurements of explant-derived TM cells may have reflected a range of responses from phenotypically different cell populations, and that the opposing effects of A 1 and A 2A agonists on outflow resistance are not likely to be mediated by actions on a single population of TM cells. These opposing effects might reflect AR responses by two or more subpopulations of TM cells, by TM and SC cells or by inner-wall SC cells, alone.

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“…The ethanol initiated increase of internal Ca 2+ , therefore, may be an additional factor to the activation of BK channels. Activation of BK channels is known to also derive from stretch activation of the cell membrane (Gasull et al, 2003;Kawakubo et al, 1999). Ethanol has been found to induce cell swelling even under isoosmotic conditions evoking transmitter and hormone secretion (Jakab et al, 2006).…”

Section: Ethanol -Bk Channels -And Cellular Signallingmentioning

confidence: 99%

BK Channels – Focus on Polyamines, Ethanol/Acetaldehyde and Hydrogen Sulfide (H2S)

Hermann¹,

Ситдикова²,

Weiger³

2012

Patch Clamp Technique

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Cell Membrane Stretch Modulates the High-Conductance Ca²⁺-Activated K⁺Channel in Bovine Trabecular Meshwork Cells

Cited by 55 publications

References 38 publications

Tuning the mechanosensitivity of a BK channel by changing the linker length

Tuning the mechanosensitivity of a BK channel by changing the linker length

Cell-specific differential modulation of human trabecular meshwork cells by selective adenosine receptor agonists

BK Channels – Focus on Polyamines, Ethanol/Acetaldehyde and Hydrogen Sulfide (H2S)

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Cell Membrane Stretch Modulates the High-Conductance Ca2+-Activated K+Channel in Bovine Trabecular Meshwork Cells

Cited by 55 publications

References 38 publications

Tuning the mechanosensitivity of a BK channel by changing the linker length

Tuning the mechanosensitivity of a BK channel by changing the linker length

Cell-specific differential modulation of human trabecular meshwork cells by selective adenosine receptor agonists

BK Channels – Focus on Polyamines, Ethanol/Acetaldehyde and Hydrogen Sulfide (H2S)

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Product

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Cell Membrane Stretch Modulates the High-Conductance Ca²⁺-Activated K⁺Channel in Bovine Trabecular Meshwork Cells