ArticlePflugers Archiv : European journal of physiology2015
Activation of endogenously expressed ion channels by active complement in the retinal pigment epithelium.
Article in Pflugers Archiv : European journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- CR2-fH, A Targeted Inhibitor of Alternative Complement Pathway Reduces Dry AMD-Like Phenotype in AMD Patient iPSC-derived RPE Cells.Investigative ophthalmology & visual science · 2026Article
- Factor-H-related protein 1 (FHR1), a promotor of para-inflammation in age-related macular degeneration.Journal of neuroinflammation · 2025Article
- Anaphylatoxin C5a receptor signaling induces mitochondrial fusion and sensitizes retinal pigment epithelial cells to oxidative stress.Biochimica et biophysica acta. General subjects · 2023Article
- Retinal TRP channels: Cell-type-specific regulators of retinal homeostasis and multimodal integration.Progress in retinal and eye research · 2023Review
- Increased plasma level of terminal complement complex in AMD patients: potential functional consequences for RPE cells.Frontiers in immunology · 2023Article
- Complement C3 Aggravates Post-epileptic Neuronal Injury Via Activation of TRPV1.Neuroscience bulletin · 2021Article
- Mitochondrial C3a Receptor Activation in Oxidatively Stressed Epithelial Cells Reduces Mitochondrial Respiration and Metabolism.Frontiers in immunology · 2021Article
- Circadian regulation in the retina: From molecules to network.The European journal of neuroscience · 2020Review
- Anaphylatoxins Activate CaFrontiers in immunology · 2017Article
- Protective responses to sublytic complement in the retinal pigment epithelium.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- A local complement response by RPE causes early-stage macular degeneration.Human molecular genetics · 2015Article
- Regulation of surface expression of TRPV2 channels in the retinal pigment epithelium.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2015Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
Defective regulation of the alternative pathway of the complement system is believed to contribute to damage of retinal pigment epithelial (RPE) cells in age-related macular degeneration. Thus we investigated the effect of complement activation on the RPE cell membrane by analyzing changes in membrane conductance via patch-clamp techniques and Ca(2+) imaging. Exposure of human ARPE-19 cells to complement-sufficient normal human serum (NHS) (25 %) resulted in a biphasic increase in intracellular free Ca(2+) ([Ca(2+)]i); an initial peak followed by sustained Ca(2+) increase. C5- or C7-depleted sera did not fully reproduce the signal generated by NHS. The initial peak of the Ca(2+) response was reduced by sarcoplasmic Ca(2+)-ATPase inhibitor thapsigargin, L-type channel blockers (R)-(+)-BayK8644 and isradipine, transient-receptor-potential (TRP) channel blocker ruthenium-red and ryanodine receptor blocker dantrolene. The sustained phase was carried by CaV1.3 L-type channels via tyrosine-phosphorylation. Changes in [Ca(2+)]I were accompanied by an abrupt hyperpolarization, resulting from a transient increase in membrane conductance, which was absent under extracellular Ca(2+)- or K(+)-free conditions and blocked by (R)-(+)-BayK8644 or paxilline, a maxiK channel inhibitor. Single-channel recordings confirmed the contribution of maxiK channels. Primary porcine RPE cells responded to NHS in a comparable manner. Pre-incubation with NHS reduced H2O2-induced cell death. In summary, in a concerted manner, C3a, C5a and sC5b-9 increased [Ca(2+)]i by ryanodine-receptor-dependent activation of L-type channels in addition to maxi-K channels and TRP channels absent from any insertion of a lytic pore.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.