Differential expression of nuclear lamin subtypes in the neural cells of the adult rat cerebral cortex.

Differential expression of nuclear lamin subtypes in the neural cells of the adult rat cerebral cortex.
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DOI:
10.1016/j.ibror.2018.11.001
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发表时间:
2018-12
期刊:
影响因子:
2.6
通讯作者:
Yamada H
Yamada H
中科院分区:
其他
文献类型:
--
作者:
Takamori Y;Hirahara Y;Wakabayashi T;Mori T;Koike T;Kataoka Y;Tamura Y;Kurebayashi S;Kurokawa K;Yamada H

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This work demonstrates the expression patterns for lamin subtypes in neural cells in the adult rat cerebral cortex. This work demonstrates suitable fixative conditions of multiple immunostaining systems for lamins and cell-type specific marker proteins. Neural cells in the adult cerebral cortex showed heterogeneous lamin antibody labeling patterns. Lamins are type V intermediate filament proteins that are located beneath the inner nuclear membrane. In mammalian somatic cells, LMNB1 and LMNB2 encode somatic lamins B1 and B2, respectively, and the LMNA gene is alternatively spliced to generate somatic lamins A and C. Mutations in lamin genes have been linked to many human hereditary diseases, including neurodegenerative disorders. Knowledge about lamins in the nervous system has been accumulated recently, but a precise analysis of lamin subtypes in glial cells has not yet been reported. In this study we investigated the composition of lamin subtypes in neurons, astrocytes, oligodendrocyte-lineage cells, and microglia in the adult rat cerebral cortex using an immunohistochemical staining method. Lamin A was not observed in neurons and glial cells. Lamin C was observed in astrocytes, mature oligodendrocytes and neurons, but not observed in oligodendrocyte progenitor cells. Microglia also did not stain positive for lamin C which differed from macrophages, with lamin C positive. Lamin B1 and B2 were observed in all glial cells and neurons. Lamin B1 was intensely positive in oligodendrocyte progenitor cells compared with other glial cells and neurons. Lamin B2 was weakly positive in all glial cells compared to neurons. Our current study might provide useful information to reveal how the onset mechanisms of human neurodegenerative diseases are associated with mutations in genes for nuclear lamin proteins.
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发表时间: 2012-02-14
影响因子: 11.1
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