TRPV channels mediate temperature-sensing in human corneal endothelial cells

Mergler, Stefan; Valtink, Monika; Coulson‐Thomas, Vivien Jane; Lindemann, Dirk; Reinach, Peter S.; Engelmann, Katrin; Pleyer, Uwe

doi:10.1016/j.exer.2010.03.010

Cited by 66 publications

(64 citation statements)

References 53 publications

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“…In Drosophila, photoreceptors and mammalian photosensitive retinal ganglion cell phototransduction is mediated by G protein-activated phospholipase C (PLC), which generates a force in the lipid-bilayer opening TRP-Canonical channels. 23,24 Transient receptor potential V1 is expressed in human conjunctival epithelial cells (HCjEC), 25 human corneal endothelial cells, 26 corneal fibroblasts, 27 and corneal epithelial cells (HCEC) 28,29 (reviewed in Ref. 30 ).…”

Section: Methodsmentioning

confidence: 99%

Upregulation of Transient Receptor Potential Vanilloid Type-1 Channel Activity and Ca²⁺Influx Dysfunction in Human Pterygial Cells

Garreis

Schröder

Reinach

et al. 2016

Invest. Ophthalmol. Vis. Sci.

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Section: Methodsmentioning

confidence: 99%

Upregulation of Transient Receptor Potential Vanilloid Type-1 Channel Activity and Ca²⁺Influx Dysfunction in Human Pterygial Cells

Garreis

Schröder

Reinach

et al. 2016

Invest. Ophthalmol. Vis. Sci.

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“…Only a few studies have reported TRPV2 expression in ECs (Table 3) and, therefore, its function in vascular endothelium is still unclear. Due to its ability to mediate Ca 2+ inflow in ECs exposed to moderate heat, however, it might aid TRPV1 to stimulate NO synthesis and peripheral vasorelaxation at > 43 ℃ [8,284] . TRPV3: TRPV3 is a polymodal channel that may be gated by either natural compounds, such as carvacrol, eugenol, and camphor, or innocuous warm temperatures (> 30 ℃) [200] .…”

Section: Trpv2mentioning

confidence: 99%

“…Baseline mean arterial pressures are, however, not statistically different in wild-type and TRPV1 -/-mice [282,283] . Besides chemical agonists, TRPV1 may be gated by temperature higher than 40 ℃ in ECs [277,284] . This feature gives support to the hypothesis that TRPV1 contribute to peripheral vascular dilatation and high temperatures [8] .…”

Section: Trpv Channelsmentioning

confidence: 99%

“…The consequent K + efflux activates smooth muscle inwardly rectifying potassium channels (KIR) and amplifies the negative shift in VSMC VM, thereby promoting arterial relaxation [287] . In human corneal ECs, TRPV3-induced Ca 2+ entry is evoked by raising bath temperature from 25 to > 44 ℃ [284] . If present also in vascular endothelium, this feature would render the channel capable of sensing high temperatures in peripheral circulation along with TRPV1 and TRPV2.…”

Section: Trpv2mentioning

confidence: 99%

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Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Moccia

Berra‐Romani²,

Tanzi³

2012

WJBC

110

192

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A monolayer of endothelial cells (ECs) lines the lumen of blood vessels and forms a multifunctional transducing organ that mediates a plethora of cardiovascular processes. The activation of ECs from as state of quiescence is, therefore, regarded among the early events leading to the onset and progression of potentially lethal diseases, such as hypertension, myocardial infarction, brain stroke, and tumor. Intracellular Ca 2+ signals have long been know to play a central role in the complex network of signaling pathways regulating the endothelial functions. Notably, recent work has outlined how any change in the pattern of expression of endothelial channels, transporters and pumps involved in the modulation of intracellular Ca 2+ levels may dramatically affect whole body homeostasis. Vascular ECs may react to both mechanical and chemical stimuli by generating a variety of intracellular Ca 2+ signals, ranging from brief, localized Ca 2+ pulses to prolonged Ca 2+ oscillations engulfing the whole cytoplasm. The well-defined spatiotemporal profile of the subcellular Ca 2+ signals elicited in ECs by specific extracellular inputs depends on the interaction between Ca 2+ releasing channels, which are located both on the plasma membrane and in a number of intracellular organelles, and Ca 2+ removing systems. The present article aims to summarize both the past and recent literature in the field to provide a clear-cut picture of our current knowledge on the molecular nature and the role played by the components of the Ca 2+ machinery in vascular ECs under both physiological and pathological conditions.

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“…RuR is considered a general noncompetitive antagonist channel blocker that interferes with the pore complex, and it is widely applied in studies of transient receptor potential vanilloid (TRPV) ion channel family members, 45 critical contributors to the perception of various environmental stimuli and nociceptive pain that have already been demonstrated to exist in human corneal epithelial 46 and endothelial 47 cells, and very recently in human conjunctival epithelium. 48 RuR also acts on intracellular concentrations of Ca by blocking both Ca 2ϩ uptake and release from mitochondria and ryanodine-sensitive intracellular stores.…”

mentioning

confidence: 99%

Hyperosmolar Stress Upregulates HLA-DR Expression in Human Conjunctival Epithelium in Dry Eye Patients and In Vitro Models

Versura

Profazio

Schiavi

et al. 2011

Invest. Ophthalmol. Vis. Sci.

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PURPOSE.To investigate the immune response of human conjunctival epithelium to hyperosmolar stress. METHODS. Tear osmolarity was measured in 15 normal subjects and 25 dry eye (DE) patients; conjunctival imprint cytology samples were obtained at the nasal bulbar area. Subconfluent primary human conjunctival epithelial cells (pHCECs) and human conjunctival organ cultures (hCOCs), both cultured in iso-osmolar medium (305 mOsm/L), were exposed for 24 hours to media with progressively higher osmolarity, with or without the ion channel inhibitor ruthenium red (RuR). Human leukocyte antigen (HLA)-DR expression was evaluated by immunocytochemistry, on imprints from subjects, on primary human conjunctival epithelial cells, on formalin fixed-paraffin embedded hCOCs, and by RT-PCR. Statistical evaluation was performed by applying the unpaired Student's t test, as well as Spearman's rho and Pearson's r correlation coefficients (significance P Ͻ 0.05). RESULTS. HLA-DR expression increased in DE subjects with respect to control (% mean Ϯ SD, respectively, 46.16 Ϯ 7.2 vs. 7.48 Ϯ 1.14, P Ͻ 0.0001) and exhibited significantly high correlations with tear osmolarity values (r ϭ 0.614; P Ͻ 0.0001). In vitro experiments showed a progressive increase in HLA-DR expression as the osmolarity of the medium was increased from 6.75 Ϯ 1.16 (% mean Ϯ SD) in iso-osmolarcultured cells to 9.96 Ϯ 1.37 and 12.94 Ϯ 4.04 in cells cultured in, respectively, 350 and 400 mOsm/L (P Ͻ 0.05). A stepwise progressive increase was also found in hCOCs. Results were confirmed by RT-PCR. Ruthenium red significantly reduced HLA-DR expression in hyperosmolar-cultured cells. CONCLUSIONS. Data from complementary techniques demonstrate that extracellular hyperosmolarity induces HLA-DR overexpression in human conjunctival epithelial cells in both DE patients and in vitro cell culture models. (Invest Ophthalmol Vis Sci. 2011;52:5488 -5496)

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TRPV channels mediate temperature-sensing in human corneal endothelial cells

Cited by 66 publications

References 53 publications

Upregulation of Transient Receptor Potential Vanilloid Type-1 Channel Activity and Ca²⁺Influx Dysfunction in Human Pterygial Cells

Upregulation of Transient Receptor Potential Vanilloid Type-1 Channel Activity and Ca²⁺Influx Dysfunction in Human Pterygial Cells

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters

Hyperosmolar Stress Upregulates HLA-DR Expression in Human Conjunctival Epithelium in Dry Eye Patients and In Vitro Models

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TRPV channels mediate temperature-sensing in human corneal endothelial cells

Cited by 66 publications

References 53 publications

Upregulation of Transient Receptor Potential Vanilloid Type-1 Channel Activity and Ca2+Influx Dysfunction in Human Pterygial Cells

Upregulation of Transient Receptor Potential Vanilloid Type-1 Channel Activity and Ca2+Influx Dysfunction in Human Pterygial Cells

Update on vascular endothelial Ca2+signalling: A tale of ion channels, pumps and transporters

Hyperosmolar Stress Upregulates HLA-DR Expression in Human Conjunctival Epithelium in Dry Eye Patients and In Vitro Models

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Product

Resources

About

Upregulation of Transient Receptor Potential Vanilloid Type-1 Channel Activity and Ca²⁺Influx Dysfunction in Human Pterygial Cells

Upregulation of Transient Receptor Potential Vanilloid Type-1 Channel Activity and Ca²⁺Influx Dysfunction in Human Pterygial Cells

Update on vascular endothelial Ca²⁺signalling: A tale of ion channels, pumps and transporters