Stimulation of L-type Ca2+Channels by Increase of Intracellular InsP3 in Rat Retinal Pigment Epithelial Cells

Mergler, Stefan; Strauß, Olaf

doi:10.1006/exer.2001.1128

Cited by 27 publications

(22 citation statements)

References 63 publications

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“…Studies particularly investigating voltage-dependent Ca 2+ channels published by different groups revealed the functional presence of Ltype Ca 2+ channels in cultured or freshly isolated RPE cells from different species including man [10,11,[14][15][16][17][18][19][20][21]. Studies exploring the regulation of these channels have shown that L-type channels can contribute to an increase in intracellular free Ca 2+ , despite the fact that RPE cells seldom undergo changes in their membrane potential which are large enough to activate these voltage-dependent channels [22]. This is enabled by phosphorylation-dependent regulation of these channels, leading to shifts in their voltage-dependent activation to more negative potentials, closer to the resting potential of RPE cells.…”

Section: Introductionmentioning

confidence: 99%

Expression profile of voltage-dependent Ca2+ channel subunits in the human retinal pigment epithelium

Wimmers

Coeppicus

Rosenthal

et al. 2008

Graefes Arch Clin Exp Ophthalmol

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Section: Introductionmentioning

confidence: 99%

Expression profile of voltage-dependent Ca2+ channel subunits in the human retinal pigment epithelium

Wimmers

Coeppicus

Rosenthal

et al. 2008

Graefes Arch Clin Exp Ophthalmol

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“…Direct addition of IP3 into the cytoplasm of RPE cells promotes the activation of Cl − currents [119]. Moreover, increase in IP3 is also known to promote the stimulation of L-type VDCC in RPE cells [102]. The increase in intracellular Ca 2+ , due to both, the release from intracellular stores and IP3-mediated stimulation of VDCCs, is expected to promote the opening of BEST-1 Cl − channels in the basolateral membrane of the RPE.…”

Section: Best-1mentioning

confidence: 98%

“…11.13). Cells maintain a resting membrane potential between −40 and −45 mV and are subject neither to extreme shifts in membrane voltage nor action potential excitability [101,102]. At the apical surface of the RPE are voltage-dependent Cl − channels that are found in association with bumetanide-sensitive Na -sensitive inward rectifying K + conductance, and aquaporins [179].…”

Section: Best-1mentioning

confidence: 99%

Pediatric Hereditary Macular Degenerations

2010

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“…Investigation revealed that freshly isolated or cultured RPE cells could express voltage-dependent L-type calcium channels [28][29][30], which can be activated by PKC [31]. Strauss et al [31] mentioned in their study that inhibition of PKC by myristoylated PKC substrate led to a fast rundown of L-type calcium channels.…”

Section: Discussionmentioning

confidence: 99%

The Inhibition of Ca<sup>2+</sup> Influx Induced by Hypericin in Cultured Human Retinal Pigment Epithelial Cells Analyzed by Confocal Imaging

Gao

Ge²

2005

Ophthalmic Res

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Purpose: Hypericin, a specific inhibitor of protein kinase C, has been reported to have potential as a therapeutic drug for proliferative vitreoretinopathy (PVR) in vitro and in vivo. In the present studies, we analyzed the dynamic changes in Ca²⁺ influx and free intracellular Ca²⁺ concentration ([Ca²⁺]_i) of cultured human retinal pigment epithelial (RPE) cells after stimulation with hypericin in an attempt to elucidate its mechnism as a therapeutic drug for PVR. Methods: RPE cells were plated in a special plastic dish and then stimulated with 100 nM phorbol-12-myristate-13-acetate (PMA) and/or 6 hypericin concentrations (0.5, 1, 2, 3, 4 and 5 µM), after which Ca²⁺ influx and [Ca²⁺]_i were determined using the fluorescence Ca²⁺ dye fluo-3 AM and laser scanning confocal microscopy. Results: The fluorescence in resting RPE cells was strong and distributed throughout the cells. The nucleus appeared more fluorescent than the cytoplasm. After stimulation with 0.5 µM hypericin, no obvious change of Ca²⁺ influx and [Ca²⁺]_i was observed. In contrast, stimulation with higher concentrations of hypericin (1–5 µM) led to a rapid decrease in Ca²⁺ influx and [Ca²⁺]_i, which was significantly different from those detected without hypericin (control experiments). In addition, no significant differences in [Ca²⁺]_i were found between 1 and 5 µM hypericin used. Stimulation with hypericin, which was applied immediately after preincubation with PMA for 24 h did not further change Ca²⁺ influx and [Ca²⁺]_i. Conclusion: In RPE cells, high concentrations of hypericin (1–5 µM) significantly inhibit Ca²⁺ influx and induce a decrease in [Ca²⁺]_i. Therefore, hypericin has potential as a therapeutic drug for PVR maybe through its inhibition of the Ca²⁺ influx pathway.

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Stimulation of L-type Ca2+Channels by Increase of Intracellular InsP3 in Rat Retinal Pigment Epithelial Cells

Cited by 27 publications

References 63 publications

Expression profile of voltage-dependent Ca2+ channel subunits in the human retinal pigment epithelium

Expression profile of voltage-dependent Ca2+ channel subunits in the human retinal pigment epithelium

Pediatric Hereditary Macular Degenerations

The Inhibition of Ca<sup>2+</sup> Influx Induced by Hypericin in Cultured Human Retinal Pigment Epithelial Cells Analyzed by Confocal Imaging

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