Cloning and Functional Expression of a Swelling-Induced Chloride Conductance Regulatory Protein, plCln, from Rabbit Ocular Ciliary Epithelium

Wan, Xiao Lin; Chen, Shan; Sears, Marvin L.

doi:10.1006/bbrc.1997.7523

Cited by 5 publications

(3 citation statements)

References 25 publications

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“…Ciliary epithelial cells have been reported to express transcripts for ClC‐3, and electrophysiological and volumetric evidence supports the association of ClC‐3 with Cl − transport by human NPCE cells (Coca‐Prados et al 1996). The cDNA encoding the protein pI Cln , thought to be a swelling‐induced chloride conductance regulatory protein, was also cloned from both rabbit ciliary epithelium (Chen et al 1998; Wan et al 1997) and human NPCE cells lines (Coca‐Prados et al 1996). Although recent data from other cell types as well as oocyte expression systems, have failed to support the concept that pI Cln is the volume‐activated Cl − channel (Voets et al 1996), overexpression of pI Cln protein from the ciliary body in oocytes resulted in outwardly rectifying current, and thus supports a role for pI Cln as a Cl − conductance regulatory protein related to Cl − channel activation in ciliary epithelial cells (Chen et al 1998).…”

Section: Discussionmentioning

confidence: 99%

Hyposmotically activated chloride channels in cultured rabbit non‐pigmented ciliary epithelial cells

Shi

Ryan

French

et al. 1999

The Journal of Physiology

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The ciliary body epithelium (CBE) forms the inner surface covering of the ciliary processes of the eye and is composed of two different epithelial cell layers: a non-pigmented ciliary epithelial (NPCE) cell layer and a pigmented ciliary epithelial (PCE) cell layer (Caprioli, 1992). Both PCE and NPCE cells are involved in the production of aqueous humour, an isotonic solution composed primarily of water, Na¤, Cl¦ and HCO×¦. The balance between the rate and quantity of aqueous humour produced and aqueous humour escape from the eye, via drainage pathways, is the primary determinant of intraocular pressure (IOP), and is subject to autonomic modulation (Caprioli, 1992). Transport data from intact and dispersed ciliary epithelial tissue suggest that PCE cells have solute uptake properties and are functionally coupled to the NPCE cells which have solute efflux properties (Wiederholt et al. 1991;Edelman et al. 1994). In this cell coupled model, ions and water from the stroma are taken up by PCE cells and passed to the NPCE cells via apical gap junctions (Raviola & Raviola, 1978), where they are secreted at the basolateral membrane into the posterior chamber as aqueous humour. Despite our understanding of this functional coupling between CE cells, the exact cellular transport mechanisms involved in fluid and ion secretion remain unresolved. However, it has now been shown that Na¤, K¤ and Cl¦ enter PCE cells via a furosemide-(frusemide-) and bumetamidesensitive Na¤-K¤-2Cl¦ symport and diffuse from PCE to NPCE cells via the apical gap junctions. Na¤, K¤ and Cl¦ ions are then secreted from NPCE cells through Na¤-K¤ exchange pumps and via basolateral K¤ and Cl¦ channels, and this is accompanied by paracellular Na¤ movement. A HCO×¦-dependent transepithelial potential of approximately

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Section: Discussionmentioning

confidence: 99%

Hyposmotically activated chloride channels in cultured rabbit non‐pigmented ciliary epithelial cells

Shi

Ryan

French

et al. 1999

The Journal of Physiology

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“…Decreased mRNA levels of chloride ion current inducer were detected after 60 and 120 min of normoxic perfusion. This gene has already been studied in rat brain and myocardium, but the gene function only described in ocular ciliary epithelium (Anguita, Chalfant, Civan, Coca-Prados , 1995;Wan, Chen, & Sears, 1997).…”

Section: Gene Expression Alteration Due To Perfusionmentioning

confidence: 99%

Gene and protein expression changes in response to normoxic perfusion in mouse hearts

Faragó

Kocsis

Feher

et al. 2008

Journal of Pharmacological and Toxicological Methods

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Introduction: Although crystalloid-perfused isolated heart models are widely used in cardiovascular research, there are several limitations of these techniques. Changes in cardiac gene expression pattern due to normoxic perfusion itself have not been studied, despite its potential importance to provide useful information on limitations of this model. Therefore, here we investigated the time-dependent effect of normoxic, normothermic perfusion on global gene expression at mRNA and protein levels. Methods: Hearts from male CFLP mice were perfused according to the Langendorff technique. We assessed relative gene expression changes by DNA microarray analysis of 8000 genes after 0, 60 and 120 min perfusion. Results: Twelve genes exhibited significant up-regulation and 27 showed repression in hearts perfused for 60 or 120 min as compared to 0 min controls. Expression changes of 17 selected genes were verified and an additional 19 genes were examined by real-time quantitative PCR. Genes with altered expression included those coding for Creatin kinase, Lactate dehydrogenase, Voltage-dependent anion channel 1, a Disintegrin and Metalloprotease domain 3, Integrin alpha 7, Long-chain acyl-CoA dehydrogenase, Casein kinase II, Ketohexokinase, Chloride ion current inducer protein, Matrix metalloproteinase 2 and 9, Superoxide dismutases and Nitric oxide synthases, etc. Discussion: Our results show that normoxic crystalloid perfusion itself results in time-dependent changes in cardiac gene expression which should be considered when designing ex vivo perfusion protocols in the mouse heart to mimic cardiac pathologies as many of these genes have been suspected to influence several cardiovascular diseases.

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“…A number of different Cl channel candidates and regulators have been proposed to underlie NPE cell I Cl,swell (Jacob and Civan 1996), including pICln (Coca-Prados et al 1995;Wan et al 1997;Chen et al 1998), the multidrug-resistant transporter P-glycoprotein (Wu et al 1996;Wang et al 1998), andClC-3 (Coca-Prados et al 1996;Wang et al 2000). Of these, only ClC-3, a member of the ClC family of Cl channels that also includes osmosensitive ClC-2 channels, still remains as a putative candidate contributing to I Cl,swell in NPE cells.…”

Section: Introductionmentioning

confidence: 99%

Hyposmotic activation of I_Cl,swell in rabbit nonpigmented ciliary epithelial cells involves increased ClC-3 trafficking to the plasma membrane

Vessey

Shi²,

Jollimore³

et al. 2004

Biochem. Cell Biol.

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In mammalian nonpigmented ciliary epithelial (NPE) cells, hyposmotic stimulation leading to cell swelling activates an outwardly rectifying Cl(-) conductance (I(Cl,swell)), which, in turn, results in regulatory volume decrease. The aim of this study was to determine whether increased trafficking of intracellular ClC-3 Cl channels to the plasma membrane could contribute to the I(Cl,swell) following hyposmotic stimulation. Our results demonstrate that hyposmotic stimulation reversibly activates an outwardly rectifying Cl(-) current that is inhibited by phorbol-12-dibutyrate and niflumic acid. Transfection with ClC-3 antisense, but not sense, oligonucleotides reduced ClC-3 expression as well as I(Cl,swell). Intracellular dialysis with 2 different ClC-3 antibodies abolished activation of I(Cl,swell). Immunofluorescence microscopy showed that hyposmotic stimulation increased ClC-3 immunoreactivity at the plasma membrane. To determine whether this increased expression of ClC-3 at the plasma membrane could be due to increased vesicular trafficking, we examined membrane dynamics with the fluorescent membrane dye FM1-43. Hyposmotic stimulation rapidly increased the rate of exocytosis, which, along with ICl,swell, was inhibited by the phosphoinositide-3-kinase inhibitor wortmannin and the microtubule disrupting agent, nocodazole. These findings suggest that ClC-3 channels contribute to I(Cl,swell) following hyposmotic stimulation through increased trafficking of channels to the plasma membrane.

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Cloning and Functional Expression of a Swelling-Induced Chloride Conductance Regulatory Protein, plCln, from Rabbit Ocular Ciliary Epithelium

Cited by 5 publications

References 25 publications

Hyposmotically activated chloride channels in cultured rabbit non‐pigmented ciliary epithelial cells

Hyposmotically activated chloride channels in cultured rabbit non‐pigmented ciliary epithelial cells

Gene and protein expression changes in response to normoxic perfusion in mouse hearts

Hyposmotic activation of I_Cl,swell in rabbit nonpigmented ciliary epithelial cells involves increased ClC-3 trafficking to the plasma membrane

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Cloning and Functional Expression of a Swelling-Induced Chloride Conductance Regulatory Protein, plCln, from Rabbit Ocular Ciliary Epithelium

Cited by 5 publications

References 25 publications

Hyposmotically activated chloride channels in cultured rabbit non‐pigmented ciliary epithelial cells

Hyposmotically activated chloride channels in cultured rabbit non‐pigmented ciliary epithelial cells

Gene and protein expression changes in response to normoxic perfusion in mouse hearts

Hyposmotic activation of ICl,swell in rabbit nonpigmented ciliary epithelial cells involves increased ClC-3 trafficking to the plasma membrane

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Hyposmotic activation of I_Cl,swell in rabbit nonpigmented ciliary epithelial cells involves increased ClC-3 trafficking to the plasma membrane