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Andreas Bringmann, Thomas Pannicke, Vanessa Moll, Ivan Milenkovic, Frank Faude, Volker Enzmann, Sebastian Wolf, Andreas Reichenbach; Upregulation of P2X7 Receptor Currents in Müller Glial Cells during Proliferative Vitreoretinopathy. Invest. Ophthalmol. Vis. Sci. 2001;42(3):860-867.
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purpose. Müller glial cells from the human retina express purinergic P2X7 receptors. Because extracellular adenosine triphosphate (ATP) is
assumed to be a mediator of the induction or maintenance of gliosis,
this study was undertaken to determine whether the expression of these
receptors is different in human Müller cells obtained from
retinas of healthy donors and of patients with choroidal melanoma and
proliferative vitreoretinopathy (PVR).
methods. Human Müller cells were enzymatically isolated from donor
retinas, and whole-cell patch-clamp recordings were made to
characterize the density of the P2X7 currents and the
activation of currents through Ca2+-activated
K+ channels of big conductance
(I BK) that reflects the increase of the
intracellular Ca2+ concentration.
results. Stimulation by external ATP or by benzoylbenzoyl ATP (BzATP) evoked
both release of Ca2+ from thapsigargin-sensitive
intracellular stores and opening of Ca2+-permeable
P2X7 channels. These responses caused transient and
sustained increases in I BK. In Müller
cells from patients with PVR, the mean density of the BzATP-evoked
cation currents was significantly greater compared with cells from
healthy donors. As a consequence, such cells displayed an enlarged I BK during application of purinergic
agonists. ATP and BzATP increased the DNA synthesis rate of cultured
cells. This effect could be reversed by blocking the I BK.
conclusions. The increased density of P2X7 receptor channels may permit
a higher level of entry of extracellular Ca2+ into cells
from patients with PVR. Enhanced Ca2+ entry and the
subsequent stronger activation of I BK may
contribute to the induction or maintenance of proliferative activity in
gliotic Müller cells during PVR.
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