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Y1 receptor of neuropeptide Y as a glial marker in proliferative vitreoretinopathy and diseased human retina
Author(s) -
Soler M. Valeria Cantó,
Gallo Juan E.,
Dodds Ricardo A.,
Hökfelt Tomas,
Villar Marcelo J.,
Suburo Angela M.
Publication year - 2002
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.10107
Subject(s) - biology , proliferative vitreoretinopathy , retina , neuropeptide y receptor , neuropeptide , neuroscience , receptor , retinal , genetics , botany , retinal detachment
The Y1 receptor of neuropeptide Y (NPY) has been demonstrated in glial cells of astrocytic lineage in vitro. We have studied the immunohistochemical expression of Y1 receptors in the glia of the diseased human retina, in tissue samples obtained after surgery for proliferative vitreoretinopathy. In this condition, glia and other cell types migrate and form epi‐ or subretinal membranes. Both diseased retinas (n = 8) and PVR membranes (n = 43) contained numerous Y1‐immunoreactive cells. In the diseased retina, the Y1 antiserum labeled cells with the morphological radial pattern characteristic of Müller cells, whereas in the membranes, label appeared in a large population of elongate cells, measuring up to 250 μm. In both retina and membranes, double labeling demonstrated that the vast majority of Y1‐immunoreactive cells were also labeled by a glial fibrillary acidic protein (GFAP) antibody, indicating their glial origin. Retinal regions devoid of GFAP immunoreactivity also lacked the Y1 label. None of these markers was detected in Müller cells of normal retina. Y1 immunoreactivity did not co‐localize with smooth muscle actin immunoreactivity, a marker of myofibroblasts. Expression of Y1 receptors would characterize reactive and proliferating glial cells of the diseased retina and could perhaps be involved in the proliferation of injured glial cells causing regrowth of PVR membranes and the consequent secondary retinal detachments. GLIA 39:320–324, 2002. © 2002 Wiley‐Liss, Inc.