NDA
Bejelentkezés
Kapcsolat
Accumulation of lipid inclusions in astrocytes of aging human optic nerve |
Tartalom: | http://real.mtak.hu/72407/ |
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Archívum: | MTA Könyvtár |
Gyűjtemény: |
Status = Published
Type = Article |
Cím: |
Accumulation of lipid inclusions in astrocytes of aging human optic nerve
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Létrehozó: |
Nag, T.
Wadhwa, Shashi
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Kiadó: |
Akadémiai Kiadó
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Dátum: |
2012
info:eu-repo/date/embargoEnd/2032-03-31
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Téma: |
QH Natural history / természetrajz
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Tartalmi leírás: |
We examined age-related changes in the human optic nerve (ON) from 10 postmortem donor eye samples (age: 21- to 94-year-old). In aged ON, many axons showed paucity of cytoskeleton, and possessed disorganized myelin that remained in the extracellular space. Lipid inclusions were detected in glia, as stained by oil red O, and these accumulated with aging. To identify and confirm which glial cell type possessed lipid inclusions, we performed immunohistochemistry (IHC) and transmission electron microscopy (TEM). Comparisons were made from TEM features and size of the glia immunolabeled with glial fibrillary acidic protein and glutamine synthetase (markers for astrocytes) and 2′,3′-cyclic nucleotide 3′-phosphodiesterase (a marker for oligodendrocytes). It was found that lipid inclusions were restricted to the astrocytes having larger perikarya than the oligodendrocytes (IHC) and possessing filaments in cytoplasm (TEM). These astrocytes also possessed myelin debris and it is thus likely that those inclusions originated from degenerated myelin of the ON axons. These data indicate that astrocytes play a role in phagocytosis and clearance of disorganized myelin in aging human ON.
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Nyelv: |
magyar
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Típus: |
Article
PeerReviewed
info:eu-repo/semantics/article
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Formátum: |
text
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Azonosító: |
Nag, T. and Wadhwa, Shashi (2012) Accumulation of lipid inclusions in astrocytes of aging human optic nerve. Acta Biologica Hungarica, 63 (Supple). pp. 54-64. ISSN 0236-5383
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Kapcsolat: |
https://doi.org/10.1556/ABiol.63.2012.Suppl.1.6
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Létrehozó: |
info:eu-repo/semantics/embargoedAccess
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