Glial fibrillary acidic protein (GFAP) in ependymal cells during development. An immunocytochemical study

Roessmann, Uros; Velasco, Manuel E.; Sindely, Stephen D.

doi:10.1016/0006-8993(80)91090-2

Cited by 198 publications

(75 citation statements)

References 25 publications

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“…25 Ependymal cell GFAP immunoreactivity disappears by adulthood in man. 20 In our study, normal brain ependymal GFAP immunoreactivity decreased on day 35 postnatally. The same pattern was also seen in experimental animals where ependymal GFAP-IR declined by 65% on day 35.…”

Section: Discussionsupporting

confidence: 58%

“…16,17 GFAP production begins as early as 25 weeks in normal human astrocytes 18 and as early as 15 weeks in ependymal cells following brain damage in utero. 19,20 In the murine brain, GFAP staining of astrocytes appears on embryonic day 18 to P0 with a subsequent rise by 2 weeks and later plateau by 1 month. Astrocytes bearing GFAP immunoreactivity serve many functions in health and disease including guidance of neuronal migration, production of extracellular matrix proteins and adhesion molecules, 21,22 production of neurite promoting factors, cerebral angiogenesis, neurotransmission, regulation of pH and ion concentration, phagocytosis, glutathione production and neuroendocrine functions.…”

Section: Discussionmentioning

confidence: 99%

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Human influenza viral infection in utero alters glial fibrillary acidic protein immunoreactivity in the developing brains of neonatal mice

et al. 2002

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Epidemiological reports describe a strong association between prenatal human influenza viral infection and later development of schizophrenia. Postmodern human brain studies, however, indicate a lack of gliosis in schizophrenic brains presumably secondary to absence of glial cells during the second trimester viral infection in utero. We hypothesized that human influenza infection in day 9 pregnant mice would alter the expression of glial fibrillary acidic protein (GFAP, an important marker of gliosis, neuron migration, and reactive injury) in developing brains of postnatal days 0, 14 and 35 mice. Determination of cellular GFAP immunoreactivity (IR) expressed as cell density in cortex and hippocampus of control and experimental brains showed increases in GFAP-positive density in exposed cortical (P = 0.03 day 14 vs control) and hippocampal cells (P = 0.035 day 14, P = 0.034 day 35). Similarly, ependymal cell layer GFAP-IR cell counts showed increases with increasing brain age from day 0, to days 14 and 35 in infected groups (P = 0.037, day 14) vs controls. The GFAP-positive cells in prenatally exposed brains showed 'hypertrophy' and more stellate morphology. These results implicate a significant role of prenatal human influenza viral infection on subsequent gliosis, which persists throughout brain development in mice from birth to adolescence.

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Section: Discussionsupporting

confidence: 58%

Section: Discussionmentioning

confidence: 99%

Human influenza viral infection in utero alters glial fibrillary acidic protein immunoreactivity in the developing brains of neonatal mice

et al. 2002

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“…of the spinal cord, are very active in cell proliferation in fetal and newborn rat but not in adult rat (Bruni et al, 1985). These cells differentiate until a certain period after birth (Bruni et al, 1983;Roessmann et al, 1980;Walsh et al, 1978). For example, ependymal cells of rat brain show many mitotic figures until 10 days after birth (Walsh et al.…”

Section: Discussionmentioning

confidence: 99%

Localization of metallothionein in the brain of rat and mouse.

Nishimura¹,

Nishimura²,

Abdel-Ghaffar³

et al. 1992

J Histochem Cytochem.

109

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Metallothionein (MT) is a low molecular mass protein inducible by heavy metals such as cadmium (Cd), zinc, and copper, and having high affiity for these metals. In the present study, we investigated the immunohistological localization of MT in the brains of rats and mice. In adult rat brain, almost no MT immunostaining was observed, whereas in adult mouse brain strong MT immunostaining was found in the ependymal cells, some glial cells, arachnoid, and pia mater. No immunostahhg was detected in neurons and endothelial cells. In younger rats (1-3 weeks old), strong MT immunostaining was observed in ependymal cells, choroid plexus epithelium, arachnoid, and pia mater. The overall MT concentration in adult mouse brain appeared higher than that of the brains of young and adult rats. When adult rats

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“…Such spots were not detectable in the fundus of 1-month-old KK mice (data not shown). Because the observation of autofluorescent spots by SLO can be attributable to possible inflammatory activation in retinas of EK and KK mice (39, 40), we used immunohistochemistry to label and identify activated Müller cells with glial fibrillary acidic protein (GFAP) (41,42) and macrophage/ microglia cells with ionized Ca 2+ -binding adaptor molecule 1 (Iba1) (43). We found massive Müller cell activation in 1-monthold KK mouse retina, as evidenced by increased GFAP staining ( Figure 9C).…”

Section: Figurementioning

confidence: 99%

Autosomal recessive retinitis pigmentosa E150K opsin mice exhibit photoreceptor disorganization

et al. 2012

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The pathophysiology of the E150K mutation in the rod opsin gene associated with autosomal recessive retinitis pigmentosa (arRP) has yet to be determined. We generated knock-in mice carrying a single nucleotide change in exon 2 of the rod opsin gene resulting in the E150K mutation. This novel mouse model displayed severe retinal degeneration affecting rhodopsin's stabilization of rod outer segments (ROS). Homozygous E150K (KK) mice exhibited early-onset retinal degeneration, with disorganized ROS structures, autofluorescent deposits in the subretinal space, and aberrant photoreceptor phagocytosis. Heterozygous (EK) mice displayed a delayed-onset milder retinal degeneration. Further, mutant receptors were mislocalized to the inner segments and perinuclear region. Though KK mouse rods displayed markedly decreased phototransduction, biochemical studies of the mutant rhodopsin revealed only minimally affected chromophore binding and G protein activation. Ablation of the chromophore by crossing KK mice with mice lacking the critical visual cycle protein LRAT slowed retinal degeneration, whereas blocking phototransduction by crossing KK mice with GNAT1-deficient mice slightly accelerated this process. This study highlights the importance of proper higherorder organization of rhodopsin in the native tissue and provides information about the signaling properties of this mutant rhodopsin. Additionally, these results suggest that patients heterozygous for the E150K mutation should be periodically reevaluated for delayed-onset retinal degeneration.

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Glial fibrillary acidic protein (GFAP) in ependymal cells during development. An immunocytochemical study

Cited by 198 publications

References 25 publications

Human influenza viral infection in utero alters glial fibrillary acidic protein immunoreactivity in the developing brains of neonatal mice

Human influenza viral infection in utero alters glial fibrillary acidic protein immunoreactivity in the developing brains of neonatal mice

Localization of metallothionein in the brain of rat and mouse.

Autosomal recessive retinitis pigmentosa E150K opsin mice exhibit photoreceptor disorganization

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