May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Hydrogen Peroxide Induces Increase in Ca2+ Influx in Human Corneal Endothelial Cells Through L–Type Ca2+ Channel Activation
Author Affiliations & Notes
  • S. Mergler
    Med. Klinik m.S. Hepatologie u. Gastroenterologie,
    Augenklinik,
    Charité – Universitätsmedizin Berlin, CVK, Berlin, Germany
  • P. Reinach
    SUNY, College of Optometry, Biological Sciences, The State University of New York, New York, NY
  • T. Yousif
    Augenklinik,
    Charité – Universitätsmedizin Berlin, CVK, Berlin, Germany
  • J. Bednarz
    Klinik und Poliklinik für Augenheilkunde, Universitätsklinikum Hamburg Eppendorf, Hamburg, Germany
  • K. Engelmann
    Augenklinik, Universitätsklinikum Carl Gustav Carus and der TU Dresden, Dresden, Germany
  • H. Dannowski
    Max–Delbrück–Centrum für Molekulare Medizin Berlin–Buch, Humboldt Universität Berlin, Berlin, Germany
  • C. Hartmann
    Augenklinik,
    Charité – Universitätsmedizin Berlin, CVK, Berlin, Germany
  • U. Pleyer
    Augenklinik,
    Charité – Universitätsmedizin Berlin, CVK, Berlin, Germany
  • Footnotes
    Commercial Relationships  S. Mergler, None; P. Reinach, None; T. Yousif, None; J. Bednarz, None; K. Engelmann, None; H. Dannowski, None; C. Hartmann, None; U. Pleyer, None.
  • Footnotes
    Support  NIH Grant EY04795, DFG Pl 150/11–1
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 4510. doi:
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      S. Mergler, P. Reinach, T. Yousif, J. Bednarz, K. Engelmann, H. Dannowski, C. Hartmann, U. Pleyer; Hydrogen Peroxide Induces Increase in Ca2+ Influx in Human Corneal Endothelial Cells Through L–Type Ca2+ Channel Activation . Invest. Ophthalmol. Vis. Sci. 2005;46(13):4510.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: During human eye bank storage, corneal endothelial function may be compromised by endogenously generated hydrogen peroxide (H2O2). To determine whether the observed decline in endothelial cell density during organ culture could be associated with H2O2 –induced increases in intracellular calcium concentration ([Ca2+]i), we characterized its dose dependent effects on the concentration of this second messenger. Methods: [Ca2+]i levels were determined in fura2–loaded human corneal endothelial (HCEC–SV40) cells using a fluorescence video imaging system. Values are expressed as means ± SEM. Results: 1 mM H2O2 transiently increased basal [Ca2+]i from 111 ± 4 nM to a peak level of 255 ± 26 nM (n = 7). With the L–type channel agonist, BayK8644 (5 µM), this effect was enhanced to 355 ± 22 nM (n = 4) even with 0.1 mM H2O2. In contrast, the L–type channel blocker, nifedipine (5 µM), suppressed the 0.1 mM H2O2 induced Ca2+ since it rose only to 116 ± 4 nM (n = 3). Conclusions: H2O2–induced increase in Ca2+ influx in HCEC occurs through L–type Ca2+ channels. Therefore, strategies that suppress L–type channel activation may extend corneal viability during eye bank storage.

Keywords: cornea: endothelium • calcium • ion channels 
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