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483 results on '"Woo, Sun-Hee"'

163. Shear stress activates monovalent cation channel transient receptor potential melastatin subfamily 4 in rat atrial myocytes via type 2 inositol 1,4,5-trisphosphate receptors and Ca2+ release.

Author

Son, Min‐Jeong, Kim, Joon‐Chul, Kim, Sung Woo, Chidipi, Bojjibabu, Muniyandi, Jeyaraj, Singh, Thoudam Debraj, So, Insuk, Subedi, Krishna P., and Woo, Sun‐Hee

Subjects
SHEARING force, MONOVALENT cations, MUSCLE cells, CALCIUM ions, LABORATORY rats
Abstract

Key points During each contraction and haemodynamic disturbance, cardiac myocytes are subjected to fluid shear stress as a result of blood flow and the relative movement of sheets of myocytes., The present study aimed to characterize the shear stress-sensitive membrane current in atrial myocytes using the whole-cell patch clamp technique, combined with pressurized fluid flow, as well as pharmacological and genetic interventions of specific proteins., The data obtained suggest that shear stress indirectly activates the monovalent cation current carried by transient receptor potential melastatin subfamily 4 channels via type 2 inositol 1,4,5-trisphosphate receptor-mediated Ca2+ release in subsarcolemmal domains of atrial myocytes., Ca2+-mediated interactions between these two proteins under shear stress may be an important mechanism by which atrial cells measure mechanical stress and translate it to alter their excitability., Abstract Atrial myocytes are subjected to shear stress during the cardiac cycle under physiological or pathological conditions. The ionic currents regulated by shear stress remain poorly understood. We report the characteristics, molecular identity and activation mechanism of the shear stress-sensitive current ( Ishear) in rat atrial myocytes. A shear stress of ∼16 dyn cm−2 was applied to single myocytes using a pressurized microflow system, and the current was measured by whole-cell patch clamp. In symmetrical CsCl solutions with minimal concentrations of internal EGTA, Ishear showed an outwardly rectifying current-voltage relationship (reversal at −2 mV). The current was conducted primarily (∼80%) by monovalent cations but not Ca2+. It was suppressed by intracellular Ca2+ buffering at a fixed physiological level, inhibitors of transient receptor potential melastatin subfamily 4 (TRPM4), intracellular introduction of TRPM4 antibodies or knockdown of TRPM4 expression, suggesting that TRPM4 carries most of this current. A notable reduction in Ishear occurred upon inhibition of Ca2+ release through the ryanodine receptors or inositol 1,4,5-trisphosphate receptors (IP3R) and upon depletion of sarcoplasmic reticulum Ca2+. In type 2 IP3R (IP3R2) knockout atrial myocytes, Ishear was 10-20% of that in wild-type myocytes. Immunocytochemistry and proximity ligation assays revealed that TRPM4 and IP3R2 were expressed at peripheral sites with co-localization, although they are not localized within 40 nm. Peripheral localization of TRPM4 was intact in IP3R2 knockout cells. The data obtained in the present study suggest that shear stress activates TRPM4 current by triggering Ca2+ release from the IP3R2 in the peripheral domains of atrial myocytes. [ABSTRACT FROM AUTHOR]

Published
2016
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164. Shear stress induces a longitudinal Ca2+ wave via autocrine activation of P2Y1 purinergic signalling in rat atrial myocytes.

Author

Kim, Joon‐Chul and Woo, Sun‐Hee

Subjects
*HEART cells, *PHYSIOLOGICAL stress, *HEMODYNAMICS, *CALCIUM ions, *RYANODINE receptors
Abstract

Key points Cardiac myocytes are subjected to fluid shear stress during the cardiac cycle and haemodynamic disturbance., A longitudinally propagating, regenerative Ca2+ wave is initiated in atrial myocytes under shear stress., Here we determine the cellular mechanism for this shear-induced Ca2+ wave using two-dimensional confocal Ca2+ imaging combined with pressurized fluid flow., Our data suggest that shear stress triggers the Ca2+ wave through ryanodine receptors via P2Y1 purinoceptor-phospholipase C-type 2 inositol 1,4,5-trisphosphate receptor signal transduction in atrial myocytes, and that this mechanotransduction is activated by gap junction hemichannel-mediated ATP release., Shear-specific mechanotransduction and the subsequent regenerative Ca2+ wave may be one way for atrial myocytes to assess mechanical stimuli directly and alter their Ca2+ signalling accordingly., Abstract Atrial myocytes are exposed to shear stress during the cardiac cycle and haemodynamic disturbance. In response, they generate a longitudinally propagating global Ca2+ wave. Here, we investigated the cellular mechanisms underlying the shear stress-mediated Ca2+ wave, using two-dimensional confocal Ca2+ imaging combined with a pressurized microflow system in single rat atrial myocytes. Shear stress of ∼16 dyn cm−2 for 8 s induced ∼1.2 aperiodic longitudinal Ca2+ waves (∼79 μm s−1) with a delay of 0.2−3 s. Pharmacological blockade of ryanodine receptors (RyRs) or inositol 1,4,5-trisphosphate receptors (IP3Rs) abolished shear stress-induced Ca2+ wave generation. Furthermore, in atrial myocytes from type 2 IP3R (IP3R2) knock-out mice, shear stress failed to induce longitudinal Ca2+ waves. The phospholipase C (PLC) inhibitor U73122, but not its inactive analogue U73343, abolished the shear-induced longitudinal Ca2+ wave. However, pretreating atrial cells with blockers for stretch-activated channels, Na+−Ca2+ exchanger, transient receptor potential melastatin subfamily 4, or nicotinamide adenine dinucleotide phosphate oxidase did not suppress wave generation under shear stress. The P2 purinoceptor inhibitor suramin, and the potent P2Y1 receptor antagonist MRS 2179, both suppressed the Ca2+ wave, whereas the P2X receptor antagonist, iso-PPADS, did not alter it. Suppression of gap junction hemichannels permeable to ATP or extracellular application of ATP-metabolizing apyrase inhibited the wave. Removal of external Ca2+ to enhance hemichannel opening facilitated the wave generation. Our data suggest that longitudinally propagating, regenerative Ca2+ release through RyRs is triggered by P2Y1-PLC-IP3R2 signalling that is activated by gap junction hemichannel-mediated ATP release in atrial myocytes under shear stress. [ABSTRACT FROM AUTHOR]

Published
2015
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176. Characterization of Peroxidase in Tartary Buckwheat Seed

Author

SUZUKI, Tatsuro, primary, SHIN, Dong-Hoon, additional, WOO, Sun-Hee, additional, MUKASA, Yuji, additional, MORISHITA, Toshikazu, additional, NODA, Takahiro, additional, TAKIGAWA, Shigenobu, additional, HASHIMOTO, Naoto, additional, YAMAUCHI, Hiroaki, additional, and MATSUURA-ENDO, Chie, additional

Published
2012
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