cDNA cloning and characterization of an osmotically sensitive TRP channel from ascidian eggs

Kondoh, Masahiro; Kasai, Takeshi; Shimada, Masumi; Kashiwayanagi, Makoto; Yokosawa, Hideyoshi

doi:10.1016/s1096-4959(02)00255-5

Cited by 7 publications

(8 citation statements)

References 15 publications

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“…Both La 3+ and Gd 3+ reduced GTTR and gentamicin uptake as expected from physiological inhibition of nonselective cationic TRP channel function in previous studies (Gillo et al, 1996;Kondoh et al, 2003;Trebak et al, 2002;Walker et al, 2002). The dose-dependent reduction of GTTR uptake by La 3+ was conWrmed by a similar reduction in the Xuorescent intensity of immunolabeled gentamicin.…”

Section: Extracellular Trivalent Cationssupporting

confidence: 56%

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TRPV1 regulators mediate gentamicin penetration of cultured kidney cells

2005

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Transient receptor potential (TRP) receptors are, typically, calcium-permeant cation channels that transduce environmental stimuli. Both kidney epithelial and inner ear sensory cells express TRPV1, are mechanosensors and accumulate the aminoglycoside antibiotic gentamicin. Recently, we showed that Texas Red-conjugated gentamicin (GTTR) enters kidney cells via an endosome-independent pathway. Here, we used GTTR to investigate this non-endocytotic mechanism of gentamicin uptake. In serum-free buffers, GTTR penetrated MDCK cells within 30 s and uptake was modulated by extracellular, multivalent cations (Ca2+, La3+, Gd3+) or protons. We verified the La3+ modulation of GTTR uptake using immunocytochemical detection of unconjugated gentamicin. Membrane depolarization, induced by high extracellular K+ or valinomycin, also reduced GTTR uptake, suggesting electrophoretic permeation through ion channels. GTTR uptake was enhanced by the TRPV1 agonists, resiniferatoxin and anandamide, in Ca2+-free media. Competitive antagonists of the TRPV1 cation current, iodo-resiniferatoxin and SB366791, also enhanced GTTR uptake independently of Ca2+, reinforcing these antagonists' potential as latent agonists in specific situations. Ruthenium Red blocked GTTR uptake in the presence or absence of these TRPV1-agonists and antagonists. In addition, GTTR uptake was blocked by RTX in the presence of more physiological levels (2 mM) of Ca2+. Thus gentamicin enters cells via cation channels, and gentamicin uptake can be modulated by regulators of the TRPV1 channel.

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Section: Extracellular Trivalent Cationssupporting

confidence: 56%

“…Gadolinium blocks calcium-permeant, mechanosensitive cation channels (Kondoh et al, 2003;Trebak et al, 2002;Urbach et al, 1999). In the absence of Gd 3+ , GTTR uptake was high (Fig.…”

Section: Extracellular Trivalent Cationsmentioning

confidence: 97%

TRPV1 regulators mediate gentamicin penetration of cultured kidney cells

2005

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“…Gd 3+ ions block calcium-permeant, mechanosensitive cation channels. 27, 28, 29 RR is also a noncompetitive TRPV antagonist that blocks numerous cation channels. GTTR uptake was clearly observed in the absence of Gd 3+ or RR.…”

Section: Resultsmentioning

confidence: 99%

Different uptake of gentamicin through TRPV1 and TRPV4 channels determines cochlear hair cell vulnerability

et al. 2013

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Hair cells at the base of the cochlea appear to be more susceptible to damage by the aminoglycoside gentamicin than those at the apex. However, the mechanism of base-to-apex gradient ototoxicity by gentamicin remains to be elucidated. We report here that gentamicin caused rodent cochlear hair cell damages in a time- and dose-dependent manner. Hair cells at the basal turn were more vulnerable to gentamicin than those at the apical turn. Gentamicin-conjugated Texas Red (GTTR) uptake was predominant in basal turn hair cells in neonatal rats. Transient receptor potential vanilloid 1 (TRPV1) and 4 (TRPV4) expression was confirmed in the cuticular plate, stereocilia and hair cell body of inner hair cells and outer hair cells. The involvement of TRPV1 and TRPV4 in gentamicin trafficking of hair cells was confirmed by exogenous calcium treatment and TRPV inhibitors, including gadolinium and ruthenium red, which resulted in markedly inhibited GTTR uptake and gentamicin-induced hair cell damage in rodent and zebrafish ototoxic model systems. These results indicate that the cytotoxic vulnerability of cochlear hair cells in the basal turn to gentamicin may depend on effective uptake of the drug, which was, in part, mediated by the TRPV1 and TRPV4 proteins.

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“…Like TRPV4, when heterologously expressed HrTRPV could mediate calcium influx in response to hypoosmolar conditions (Kondoh et al, 2003).…”

Section: Osm-9 and Ocr-2: Trpv Proteins For Polymodal Nociceptionmentioning

confidence: 99%

Invertebrate nociception: Behaviors, neurons and molecules

Tobin

Bargmann

2004

J. Neurobiol.

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Genetic analysis of nociceptive behaviors in the nematode Caenorhabditis elegans and the fruit fly Drosophila melanogaster has led to the discovery of conserved sensory transduction channels and signaling molecules. These are embedded in neurons and circuits that generate responses to noxious signals. This article reviews the neurons and molecular mechanisms that underlie invertebrate nociception. We begin with the neurobiology of invertebrate nociception, and then focus on molecules with conserved functions in vertebrate nociception and sensory biology.

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cDNA cloning and characterization of an osmotically sensitive TRP channel from ascidian eggs

Cited by 7 publications

References 15 publications

TRPV1 regulators mediate gentamicin penetration of cultured kidney cells

TRPV1 regulators mediate gentamicin penetration of cultured kidney cells

Different uptake of gentamicin through TRPV1 and TRPV4 channels determines cochlear hair cell vulnerability

Invertebrate nociception: Behaviors, neurons and molecules

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