Retinal neurodegeneration in the DBA/2J mouse-a model for ocular hypertension
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Retinal neurodegeneration in the DBA/2J mouse-a model for ocular hypertension. / Schuettauf, Frank; Rejdak, Robert; Walski, Michal; Frontczak-Baniewicz, Malgorzata; Voelker, Michael; Blatsios, Georgios; Shinoda, Kei; Zagorski, Zbigniew; Zrenner, Eberhart; Grieb, Pawel.
in: ACTA NEUROPATHOL, Jahrgang 107, Nr. 4, 04.2004, S. 352-8.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Retinal neurodegeneration in the DBA/2J mouse-a model for ocular hypertension
AU - Schuettauf, Frank
AU - Rejdak, Robert
AU - Walski, Michal
AU - Frontczak-Baniewicz, Malgorzata
AU - Voelker, Michael
AU - Blatsios, Georgios
AU - Shinoda, Kei
AU - Zagorski, Zbigniew
AU - Zrenner, Eberhart
AU - Grieb, Pawel
PY - 2004/4
Y1 - 2004/4
N2 - Mice of the DBA/2J strain spontaneously develop complex ocular abnormalities, including glaucomatous loss of retinal ganglion cells (RGC). In the present study ultrastructural features of retinal neurodegeneration in DBA/2J mice of different age (3, 6, 8 and 11 months) are described. By 3 months, RGC apoptosis characterized by electron-dense karioplasm and cytoplasm of ganglion cells was observed. The occurrence of apoptotic ganglion cells peaked at the age of 6 months. Past this age, necrosis characterized by swelling and electron-rare cytoplasm appeared to be the prevailing form of cell death. Müller glia activation increased with age, but there were no signs of leukocyte infiltration. At 8 and 11 months, signs of neoangiogenesis were found both at the ultrastructural level and in clinical examinations. In these older animals myelin-like bodies, most probably representing the intracellular aggregates of phospholipids in irreversibly injured cells, were also seen. Photoreceptor cells were not affected at any age. Our observations suggest that retinal degeneration in the DBA/2J mice does not involve recruitment of blood-borne inflammatory/phagocytosing cells, and that apoptosis is gradually replaced by necrosis as the predominant pathway of RGC death. Retinal degeneration in 3- to 11-month-old DBA/2J mice partially resembles human pigment dispersion syndrome and pigmentary glaucoma with characteristic anterior segment changes and elevation of intraocular pressure. However, neovasculogenesis and myelin-like bodies are observed during aging. Therefore, the DBA/2J model requires judicious interpretation as a glaucoma model.
AB - Mice of the DBA/2J strain spontaneously develop complex ocular abnormalities, including glaucomatous loss of retinal ganglion cells (RGC). In the present study ultrastructural features of retinal neurodegeneration in DBA/2J mice of different age (3, 6, 8 and 11 months) are described. By 3 months, RGC apoptosis characterized by electron-dense karioplasm and cytoplasm of ganglion cells was observed. The occurrence of apoptotic ganglion cells peaked at the age of 6 months. Past this age, necrosis characterized by swelling and electron-rare cytoplasm appeared to be the prevailing form of cell death. Müller glia activation increased with age, but there were no signs of leukocyte infiltration. At 8 and 11 months, signs of neoangiogenesis were found both at the ultrastructural level and in clinical examinations. In these older animals myelin-like bodies, most probably representing the intracellular aggregates of phospholipids in irreversibly injured cells, were also seen. Photoreceptor cells were not affected at any age. Our observations suggest that retinal degeneration in the DBA/2J mice does not involve recruitment of blood-borne inflammatory/phagocytosing cells, and that apoptosis is gradually replaced by necrosis as the predominant pathway of RGC death. Retinal degeneration in 3- to 11-month-old DBA/2J mice partially resembles human pigment dispersion syndrome and pigmentary glaucoma with characteristic anterior segment changes and elevation of intraocular pressure. However, neovasculogenesis and myelin-like bodies are observed during aging. Therefore, the DBA/2J model requires judicious interpretation as a glaucoma model.
KW - Age Factors
KW - Animals
KW - Disease Models, Animal
KW - Female
KW - Mice
KW - Mice, Inbred Strains
KW - Mice, Mutant Strains
KW - Microscopy, Electron/methods
KW - Neuroglia/pathology
KW - Neurons/pathology
KW - Ocular Hypertension/complications
KW - Retina/pathology
KW - Retinal Degeneration/etiology
U2 - 10.1007/s00401-003-0816-9
DO - 10.1007/s00401-003-0816-9
M3 - SCORING: Journal article
C2 - 14745571
VL - 107
SP - 352
EP - 358
JO - ACTA NEUROPATHOL
JF - ACTA NEUROPATHOL
SN - 0001-6322
IS - 4
ER -