The AMOG/β2 subunit of Na, K‐ATPase is not necessary for long‐term survival of telencephalic grafts

Isenmann, Stefan; Molthagen, Martin; Brandner, Sebastian; Bartsch, Udo; Kühne, G.; Magyar, Josef P.; Sure, Ulrich; Schachner, Melitta; Aguzzi, Adriano

doi:10.1002/glia.440150403

Cited by 18 publications

(12 citation statements)

References 41 publications

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“…Similarly, grafts of brain tissue from AMOG 0/0 mice have been shown to survive as healthy tissue in host mice for as long as 2 years, without invasion of cells expressing ␤2 (Isenmann et al, 1995). The knockout mice do die at P17-18, however, with enlarged ventricles and spongiform lesions in the brainstem representing vacuolization of astrocytes apposed to blood vessels (Magyar et al, 1994).…”

Section: Resultsmentioning

confidence: 99%

Isoforms of Na,K-ATPase α and β Subunits in the Rat Cerebellum and in Granule Cell Cultures

1997

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There are multiple isoforms of the Na,K-ATPase in the nervous system, three isoforms of the ␣ subunit, and at least two of the ␤ subunit. The ␣ subunit is the catalytic subunit. The ␤ subunit has several roles. It is required for enzyme assembly, it has been implicated in neuron-glia adhesion, and the experimental exchange of ␤ subunit isoforms modifies enzyme kinetics, implying that it affects functional properties. Here we describe the specificities of antibodies against the Na,K-ATPase ␤ subunit isoforms ␤1 and ␤2. These antibodies, along with antibodies against the ␣ subunit isoforms, were used to stain sections of the rat cerebellum and cultures of cerebellar granule cells to ascertain expression and subcellular distribution in identifiable cells. Comparison of ␣ and ␤ isoform distribution with doublelabel staining demonstrated that there was no preferential association of particular ␣ subunits with particular ␤ subunits, nor was there an association with excitatory or inhibitory neurotransmission modes. Isoform composition differences were seen when Purkinje, basket, and granule cells were compared. Whether ␤1 and ␤2 are specific for neurons and glia, respectively, has been controversial, but expression of both ␤ subunit types was seen here in granule cells. In rat cerebellar astrocytes, in sections and in culture, ␣2 expression was prominent, yet the expression of either ␤ subunit was low in comparison. The complexity of Na,K-ATPase isoform distribution underscores the subtlety of its regulation and physiological role in excitable cells.

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Section: Resultsmentioning

confidence: 99%

Isoforms of Na,K-ATPase α and β Subunits in the Rat Cerebellum and in Granule Cell Cultures

1997

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“…In contrast to photoreceptor cells, however, glial cells might still, possess sufficient amounts of ~1 protein at the time of the animal's death to express a functional Na,K-ATPase; (2) glial cells in the optic nerve express the [~l-subunit below detection level and thus express a functional Na,K-ATPase or (3) glial cells in the optic nerve express a third and yet unknown [3-for the adhesion molecule on glia 253 subunit. We consider the first possibility unlikely since forebrain anlagen from ~2-deficient mice transplanted into wild-type brains contain astrocytes having no detectable levels of [~1 expression more than 500 days after transplantation (Isenmann et al, 1995). The preparation of optic nerve glial cell cultures and subsequent PCR analysis or immunoprecipitation experiments with antibodies to ~-subunits might help to distinguish between the second or third possibility, respectively.…”

Section: O L T H a G E N S C H A C H N E R And B A R T S C Hmentioning

confidence: 98%

Apoptotic cell death of photoreceptor cells in mice deficient for the adhesion molecule on glia (AMOG, the β2-subunit of the Na,K-ATPase)

1996

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Disruption of the gene for the adhesion molecule on glia (AMOG, the beta 2-subunit of the Na, K-ATPase) in mice results in swelling and subsequent degeneration of astrocyte endfeet in the brainstem and in cell death of photoreceptor cells in the retina. In the present study, we demonstrate that photoreceptor cells in the mutant develop normally during the first postnatal week. Compared to wild-type mice, a slightly increased density of degenerating photoreceptor cells became apparent in 9-day-old mutants and numerous degenerating photoreceptor cells were present in the retina of 16-day-old AMOG/beta 2-deficient mice. In situ labelling of degenerating cells by terminal dUTP nick end labelling and electron microscopic analysis revealed apoptotic cell death of photoreceptor cells. Massive degeneration of photoreceptor cells in the mutant at postnatal day 16 correlated with elevated levels of glial fibrillary acidic protein in retinal astrocytes and with expression of this protein by Muller cells. No evidence was found for degeneration of other retinal cell types or for glial cell death in the optic nerve. Our observations demonstrate that the pathological death of cells induced by disruption of the AMOG/beta 2 gene results from activation of an intrinsic death program, similar to what has been shown to occur during normal development.

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“…Methods: mating of mice: mice heterozygous for MTF-1 were mated and the morning at which a vaginal plug was detected was defined as embryonic day E 0.5. The embryos were harvested at day E12.5, and the neuroectodermal tissue was dissected and implanted into the caudoputamen of anesthetized six week-old wild-type female mice (C57 BL/6), using a stereotaxic frame and coordinates as previously described (Isenmann et al, 1995).…”

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confidence: 99%

“…At this gestational age, the neuroectodermal brain anlage is immature, but already committed to further differentiation into neuronal and glial cells. Transplantation of such neuroectodermal stem cells into the brain of an adult wild-type mouse has been shown to faithfully recapitulate the neural differentiation and lead to mature, fully-differentiated graft tissue (Isenmann et al, 1995Brandner et al, 1996). Transplantation of neural tissue was therefore performed essentially as described (Isenmann et al, 1995.…”

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confidence: 99%

The Heavy Metal-Responsive Transcription Factor-1 (MTF-1) Is Not Required for Neural Differentiation

Lichtlen¹,

Georgiev²,

Schaffner³

et al. 1999

Biological Chemistry

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The zinc finger transcription factor MTF-1 is essential for proper response to heavy metal load and other stress conditions in vertebrates, and also contributes to the maintenance of the cellular redox state. Target genes include metallothioneins (MT-I and MT-II) and gamma-glutamylcysteine synthetase (gamma-GCS), an enzyme involved in glutathione biosynthesis. Although MTF-1 is expressed ubiquitously, the primary defect in null mutant mice is hepatocyte necrosis, which results in embryonic lethality around day E14 and prevents the analysis of delayed effects on other organs. To assess the impact of MTF-1 deficiency on the function of the mature central nervous system, we employed the neural grafting strategy. Neuroectodermal brain tissue obtained from transgenic mouse embryos at gestational day 12.5 was transplanted into the caudoputamen of adult wild-type mice. 33 days later, grafts derived from MTF-1 deficient mice consisted of fully differentiated neuroectodermal tissue and showed no differences to heterozygous control grafts. This indicates that MTF-1 is dispensable for the development and differentiation of the nervous system. Such transplants devoid of MTF-1 may provide a useful tool for the further investigation of the effect of cell stress, including oxidative stress.

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The AMOG/β2 subunit of Na, K‐ATPase is not necessary for long‐term survival of telencephalic grafts

Cited by 18 publications

References 41 publications

Isoforms of Na,K-ATPase α and β Subunits in the Rat Cerebellum and in Granule Cell Cultures

Isoforms of Na,K-ATPase α and β Subunits in the Rat Cerebellum and in Granule Cell Cultures

Apoptotic cell death of photoreceptor cells in mice deficient for the adhesion molecule on glia (AMOG, the β2-subunit of the Na,K-ATPase)

The Heavy Metal-Responsive Transcription Factor-1 (MTF-1) Is Not Required for Neural Differentiation

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