Hypotonic-induced Stretching of Plasma Membrane Activates Transient Receptor Potential Vanilloid Channels and Sodium–Calcium Exchangers in Mouse Odontoblasts

Sato, Masaki; Ubaidus, Sobhan; Tsumura, Maki; Kuroda, Hidetaka; Soya, Manabu; Masamura, Aya; Nishiyama, Akihiro; Katakura, Akira; Ichinohe, Tatsuya; Tazaki, Masakazu; Shibukawa, Yoshiyuki

doi:10.1016/j.joen.2013.01.012

Cited by 58 publications

(67 citation statements)

References 28 publications

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“…The residual component (∼40%) in the transient phase of [Ca 2+ ] i rise after RuR or tranilast treatment might be mediated by other mechanosensitive Ca 2+ -permeable channels, such as TRPC1, TRPV4, TRPM7 and TRPP2. Our data agreed with several previous reports, which showed TRPV2 being a hypotonocity-activated channel in other cell types, including murine aortic smooth muscle [25] and mouse odontoblasts [26].…”

Section: Discussionsupporting

confidence: 93%

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An Upregulation in the Expression of Vanilloid Transient Potential Channels 2 Enhances Hypotonicity-Induced Cytosolic Ca2+ Rise in Human Induced Pluripotent Stem Cell Model of Hutchinson Gillford Progeria

Tjong

et al. 2014

PLoS ONE

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Hutchinson-Gillford Progeria Syndrome (HGPS) is a fatal genetic disorder characterized by premature aging in multiple organs including the skin, musculoskeletal and cardiovascular systems. It is believed that an increased mechanosensitivity of HGPS cells is a causative factor for vascular cell death and vascular diseases in HGPS patients. However, the exact mechanism is unknown. Transient receptor potential (TRP) channels are cationic channels that can act as cellular sensors for mechanical stimuli. The aim of this present study was to examine the expression and functional role of TRP channels in human induced pluripotent stem cell-derived endothelial cells (iPSC-ECs) from the patients with HGPS. The mRNA and protein expression of TRP channels in HGPS and control (IMR90) iPSC-ECs were examined by semi-quantitative RT-PCRs and immunoblots, respectively. Hypotonicity-induced cytosolic Ca2+ ([Ca2+]i) rise in iPSC-ECs was measured by confocal microscopy. RT-PCRs and immunoblots showed higher expressional levels of TRPV2 in iPSC-ECs from HGPS patients than those from normal individuals. In functional studies, hypotonicity induced a transient [Ca2+]i rise in iPSC-ECs from normal individuals but a sustained [Ca2+]i elevation in iPSC-ECs from HGPS patients. A nonselective TRPV inhibitor, ruthenium red (RuR, 20 µM), and a specific TRPV2 channel inhibitor, tranilast (100 µM), abolished the sustained phase of hypotonicity-induced [Ca2+]i rise in iPSC-ECs from HGPS patients, and also markedly attenuated the transient phase of the [Ca2+]i rise in these cells. Importantly, a short 10 min hypotonicity treatment caused a substantial increase in caspase 8 activity in iPSC-ECs from HGPS patients but not in cells from normal individuals. Tranilast could also inhibit the hypotonicity-induced increase in caspase 8 activity. Taken together, our data suggest that an up-regulation in TRPV2 expression causes a sustained [Ca2+]i elevation in HGPS-iPSC-ECs under hypotonicity, consequently resulting in apoptotic cell death. This mechanism may contribute to the pathogenesis of vascular diseases in HGPS patients.

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Section: Discussionsupporting

confidence: 93%

“…TRPV2 has been known to be a mechanosensitive channel [25], [26]. To determine whether TRPV2 was involved in hypotonicity-induced [Ca 2+ ] i influx, a nonselective TRPV inhibitor ruthenium red (RuR) and a TRPV2-specific inhibitor tranilast were used.…”

Section: Resultsmentioning

confidence: 99%

An Upregulation in the Expression of Vanilloid Transient Potential Channels 2 Enhances Hypotonicity-Induced Cytosolic Ca2+ Rise in Human Induced Pluripotent Stem Cell Model of Hutchinson Gillford Progeria

Tjong

et al. 2014

PLoS ONE

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“…(2) Prolonged hyperosmotic stress promotes VP gene transcription and translation and RVI (Figure 1Bc) while maintaining ECM-integrin-associated gate opening. (3) Early hyposmotic tension causes mild conformational change in integrins-TRP complex, inhibition of TRPV channels by their uncoupling with microtubule network and the “leakage” of these channels (Muraki et al, 2003; Sato et al, 2013; Jo et al, 2016) including ATP. ATP activation of purine-associated opening of TRPC and other TRP channels (Goel et al, 2007; Soya et al, 2014) can quickly reverse this initial inhibition and lead to cytosolic Ca 2+ increase.…”

Section: Resultsmentioning

confidence: 99%

“…Consistently, cell shrinkage evoked with sucrose or sorbitol can also activate Swiss 3T3 cells (Lunn and Rozengurt, 2004). By contrast, cell swelling or membrane stretch following hyposmotic challenge can also activate TRP channels (Figures 1Ca,Cb), such as TRPV2 in freshly isolated cells from mouse aorta (Muraki et al, 2003), TRPV1, TRPV2 and TRPV4 in mouse odontoblasts (Sato et al, 2013), etc. Consistently, TRPC5 channels of sensory neurons can also be activated by intracellular application of steps of positive pressure through the patch pipette in the whole-cell configuration (Gomis et al, 2008).…”

Section: Cellular Volumementioning

confidence: 99%

Interactions of the Mechanosensitive Channels with Extracellular Matrix, Integrins, and Cytoskeletal Network in Osmosensation

Jiao

Cui

Wang

et al. 2017

Front. Mol. Neurosci.

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Life is maintained in a sea water-like internal environment. The homeostasis of this environment is dependent on osmosensory system translation of hydromineral information into osmotic regulatory machinery at system, tissue and cell levels. In the osmosensation, hydromineral information can be converted into cellular reactions through osmoreceptors, which changes thirst and drinking, secretion of antidiuretic vasopressin (VP), reabsorption of water and salt in the kidneys at systemic level as well as cellular metabolic activity and survival status at tissue level. The key feature of osmosensation is the activation of mechanoreceptors or mechanosensors, particularly transient receptor potential vallinoid (TRPV) and canonical (TRPC) family channels, which increases cytosolic Ca2+ levels, activates osmosensory cells including VP neurons and triggers a series of secondary reactions. TRPV channels are sensitive to both hyperosmotic and hyposmotic stimuli while TRPC channels are more sensitive to hyposmotic challenge in neurons. The activation of TRP channels relies on changes in cell volume, membrane stretch and cytoskeletal reorganization as well as hydration status of extracellular matrix (ECM) and activity of integrins. Different families of TRP channels could be activated differently in response to hyperosmotic and hyposmotic stimuli in different spatiotemporal orders, leading to differential reactions of osmosensory cells. Together, they constitute the osmosensory machinery. The activation of this osmoreceptor complex is also associated with the activity of other osmolarity-regulating organelles, such as water channel protein aquaporins, Na-K-2Cl cotransporters, volume-sensitive anion channels, sodium pump and purinergic receptors in addition to intercellular interactions, typically astrocytic neuronal interactions. In this article, we review our current understandings of the composition of osmoreceptors and the processes of osmosensation.

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“…The OLCs used in this study are positive for various odontoblast-representative transcripts such as dentin sialophosphoprotein, dentin matrix protein-1, and nestin (Arany et al, 2006; Sato et al, 2013). In the present study, BzATP, a selective agonist of P2X 7 receptor, induced inward current in odontoblasts.…”

Section: Discussionmentioning

confidence: 99%

Ionotropic P2X ATP Receptor Channels Mediate Purinergic Signaling in Mouse Odontoblasts

et al. 2017

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ATP modulates various functions in the dental pulp cells, such as intercellular communication and neurotransmission between odontoblasts and neurons, proliferation of dental pulp cells, and odontoblast differentiation. However, functional expression patterns and their biophysical properties of ionotropic ATP (P2X) receptors (P2X1–P2X7) in odontoblasts were still unclear. We examined these properties of P2X receptors in mouse odontoblasts by patch-clamp recordings. K+-ATP, nonselective P2X receptor agonist, induced inward currents in odontoblasts in a concentration-dependent manner. K+-ATP-induced currents were inhibited by P2X4 and P2X7 selective inhibitors (5-BDBD and KN62, respectively), while P2X1 and P2X3 inhibitors had no effects. P2X7 selective agonist (BzATP) induced inward currents dose-dependently. We could not observe P2X1, 2/3, 3 selective agonist (αβ-MeATP) induced currents. Amplitudes of K+-ATP-induced current were increased in solution without extracellular Ca2+, but decreased in Na+-free extracellular solution. In the absence of both of extracellular Na+ and Ca2+, K+-ATP-induced currents were completely abolished. K+-ATP-induced Na+ currents were inhibited by P2X7 inhibitor, while the Ca2+ currents were sensitive to P2X4 inhibitor. These results indicated that odontoblasts functionally expressed P2X4 and P2X7 receptors, which might play an important role in detecting extracellular ATP following local dental pulp injury.

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Hypotonic-induced Stretching of Plasma Membrane Activates Transient Receptor Potential Vanilloid Channels and Sodium–Calcium Exchangers in Mouse Odontoblasts

Cited by 58 publications

References 28 publications

An Upregulation in the Expression of Vanilloid Transient Potential Channels 2 Enhances Hypotonicity-Induced Cytosolic Ca2+ Rise in Human Induced Pluripotent Stem Cell Model of Hutchinson Gillford Progeria

An Upregulation in the Expression of Vanilloid Transient Potential Channels 2 Enhances Hypotonicity-Induced Cytosolic Ca2+ Rise in Human Induced Pluripotent Stem Cell Model of Hutchinson Gillford Progeria

Interactions of the Mechanosensitive Channels with Extracellular Matrix, Integrins, and Cytoskeletal Network in Osmosensation

Ionotropic P2X ATP Receptor Channels Mediate Purinergic Signaling in Mouse Odontoblasts

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