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

Martin Molthagen, Melitta Schachner, Udo Bartsch

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Disruption of the gene for the adhesion molecule on glia (AMOG, the β2- 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 routants and numerous degenerating photoreceptor cells were present in the retina of 16- day-old AMOG/β2-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/β2 gene results from activation of an intrinsic death program, similar to what has been shown to occur during normal development.

Original languageEnglish (US)
Pages (from-to)243-255
Number of pages13
JournalJournal of Neurocytology
Volume25
Issue number4
StatePublished - Jul 5 1996
Externally publishedYes

Fingerprint

Photoreceptor Cells
Neuroglia
Cell Death
Astrocytes
Retina
Ependymoglial Cells
Retinal Degeneration
Glial Fibrillary Acidic Protein
Optic Nerve
Transcriptional Activation
Brain Stem
sodium-translocating ATPase
Electrons
Genes
Proteins

All Science Journal Classification (ASJC) codes

  • Anatomy
  • Neuroscience(all)
  • Histology
  • Cell Biology

Cite this

@article{4d0ee3a456d0414ab5f4e05f7b46443e,
title = "Apoptotic cell death of photoreceptor cells in mice deficient for the adhesion molecule on glia (AMOG, the β2-subunit of the Na,K-ATPase)",
abstract = "Disruption of the gene for the adhesion molecule on glia (AMOG, the β2- 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 routants and numerous degenerating photoreceptor cells were present in the retina of 16- day-old AMOG/β2-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/β2 gene results from activation of an intrinsic death program, similar to what has been shown to occur during normal development.",
author = "Martin Molthagen and Melitta Schachner and Udo Bartsch",
year = "1996",
month = "7",
day = "5",
language = "English (US)",
volume = "25",
pages = "243--255",
journal = "Journal of Neurocytology",
issn = "0300-4864",
publisher = "Kluwer Academic Publishers",
number = "4",

}

Apoptotic cell death of photoreceptor cells in mice deficient for the adhesion molecule on glia (AMOG, the β2-subunit of the Na,K-ATPase). / Molthagen, Martin; Schachner, Melitta; Bartsch, Udo.

In: Journal of Neurocytology, Vol. 25, No. 4, 05.07.1996, p. 243-255.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Apoptotic cell death of photoreceptor cells in mice deficient for the adhesion molecule on glia (AMOG, the β2-subunit of the Na,K-ATPase)

AU - Molthagen, Martin

AU - Schachner, Melitta

AU - Bartsch, Udo

PY - 1996/7/5

Y1 - 1996/7/5

N2 - Disruption of the gene for the adhesion molecule on glia (AMOG, the β2- 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 routants and numerous degenerating photoreceptor cells were present in the retina of 16- day-old AMOG/β2-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/β2 gene results from activation of an intrinsic death program, similar to what has been shown to occur during normal development.

AB - Disruption of the gene for the adhesion molecule on glia (AMOG, the β2- 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 routants and numerous degenerating photoreceptor cells were present in the retina of 16- day-old AMOG/β2-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/β2 gene results from activation of an intrinsic death program, similar to what has been shown to occur during normal development.

UR - http://www.scopus.com/inward/record.url?scp=0029897527&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029897527&partnerID=8YFLogxK

M3 - Article

C2 - 8793730

AN - SCOPUS:0029897527

VL - 25

SP - 243

EP - 255

JO - Journal of Neurocytology

JF - Journal of Neurocytology

SN - 0300-4864

IS - 4

ER -