Loss of Neurons in the Hippocampus and Cerebral Cortex of AMSH-Deficient Mice

AMSH, a molecule that associates with STAM1, is involved in the in vitro cell growth signaling mediated by interleukin 2 and granulocyte-macrophage colony-stimulating factor. To investigate the in vivo functional role of AMSH, we have generated AMSH-deficient mice by gene targeting. The AMSH-deficie...

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Hlavní autoři: Ishii, Naoto, Owada, Yuji, Yamada, Mitsuhiro, Miura, Shigeto, Murata, Kazuko, Asao, Hironobu, Kondo, Hisatake, Sugamura, Kazuo
Médium: Článek
Jazyk:en
Vydáno: American Society for Microbiology 2001
Témata:
Mammalian Genetic Models with Minimal or Complex Phenotypes
On-line přístup:https://ncbi.nlm.nih.gov/pmc/articles/PMC100023/
https://ncbi.nlm.nih.gov/pubmed/11713295
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1128/MCB.21.24.8626-8637.2001
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spelling pubmed-1000232002-09-12 Loss of Neurons in the Hippocampus and Cerebral Cortex of AMSH-Deficient Mice Ishii, Naoto Owada, Yuji Yamada, Mitsuhiro Miura, Shigeto Murata, Kazuko Asao, Hironobu Kondo, Hisatake Sugamura, Kazuo Mol Cell Biol Mammalian Genetic Models with Minimal or Complex Phenotypes AMSH, a molecule that associates with STAM1, is involved in the in vitro cell growth signaling mediated by interleukin 2 and granulocyte-macrophage colony-stimulating factor. To investigate the in vivo functional role of AMSH, we have generated AMSH-deficient mice by gene targeting. The AMSH-deficient mice were morphologically indistinguishable from their littermates at birth, and histopathological examinations revealed normal morphogenesis in all tissues tested. However, all the AMSH-deficient mice exhibited postnatal growth retardation and died between postnatal day 19 (P19) and P23. Examination of brain sections at P6 demonstrated significant loss of neurons and apoptotic cells in the CA1 subfield of the hippocampus. Brain atrophy developed by P16 and was accompanied by complete loss of the CA1 neurons in the hippocampus and marked atrophy of the cerebral cortex. Furthermore, AMSH-deficient hippocampal neuronal cells were unable to survive in vitro, even in the presence of several stimulatory cytokines, while AMSH-deficient cerebellar neurons, thymocytes, and embryonic fibroblasts survived normally. Taken together, these observations indicate that AMSH is an essential molecule for the survival of neuronal cells in early postnatal mice. American Society for Microbiology 2001-12 /pmc/articles/PMC100023/ /pubmed/11713295 http://dx.doi.org/10.1128/MCB.21.24.8626-8637.2001 Text en Copyright © 2001, American Society for Microbiology
institution US National Library of Medicine
collection PubMed Central
language en
format Article
topic Mammalian Genetic Models with Minimal or Complex Phenotypes
spellingShingle Mammalian Genetic Models with Minimal or Complex Phenotypes
Ishii, Naoto
Owada, Yuji
Yamada, Mitsuhiro
Miura, Shigeto
Murata, Kazuko
Asao, Hironobu
Kondo, Hisatake
Sugamura, Kazuo
Loss of Neurons in the Hippocampus and Cerebral Cortex of AMSH-Deficient Mice
description AMSH, a molecule that associates with STAM1, is involved in the in vitro cell growth signaling mediated by interleukin 2 and granulocyte-macrophage colony-stimulating factor. To investigate the in vivo functional role of AMSH, we have generated AMSH-deficient mice by gene targeting. The AMSH-deficient mice were morphologically indistinguishable from their littermates at birth, and histopathological examinations revealed normal morphogenesis in all tissues tested. However, all the AMSH-deficient mice exhibited postnatal growth retardation and died between postnatal day 19 (P19) and P23. Examination of brain sections at P6 demonstrated significant loss of neurons and apoptotic cells in the CA1 subfield of the hippocampus. Brain atrophy developed by P16 and was accompanied by complete loss of the CA1 neurons in the hippocampus and marked atrophy of the cerebral cortex. Furthermore, AMSH-deficient hippocampal neuronal cells were unable to survive in vitro, even in the presence of several stimulatory cytokines, while AMSH-deficient cerebellar neurons, thymocytes, and embryonic fibroblasts survived normally. Taken together, these observations indicate that AMSH is an essential molecule for the survival of neuronal cells in early postnatal mice.
author Ishii, Naoto
Owada, Yuji
Yamada, Mitsuhiro
Miura, Shigeto
Murata, Kazuko
Asao, Hironobu
Kondo, Hisatake
Sugamura, Kazuo
author_facet Ishii, Naoto
Owada, Yuji
Yamada, Mitsuhiro
Miura, Shigeto
Murata, Kazuko
Asao, Hironobu
Kondo, Hisatake
Sugamura, Kazuo
author_sort Ishii, Naoto
title Loss of Neurons in the Hippocampus and Cerebral Cortex of AMSH-Deficient Mice
title_short Loss of Neurons in the Hippocampus and Cerebral Cortex of AMSH-Deficient Mice
title_full Loss of Neurons in the Hippocampus and Cerebral Cortex of AMSH-Deficient Mice
title_fullStr Loss of Neurons in the Hippocampus and Cerebral Cortex of AMSH-Deficient Mice
title_full_unstemmed Loss of Neurons in the Hippocampus and Cerebral Cortex of AMSH-Deficient Mice
title_sort loss of neurons in the hippocampus and cerebral cortex of amsh-deficient mice
publisher American Society for Microbiology
publisher_facet American Society for Microbiology
publishDate 2001
url https://ncbi.nlm.nih.gov/pmc/articles/PMC100023/
https://ncbi.nlm.nih.gov/pubmed/11713295
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1128/MCB.21.24.8626-8637.2001
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