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Accelerated aging of dermal fibroblast-like cells from senescence-accelerated mouse (SAM). 1. Acceleration of population aging in vitro.

作者信息

Hosokawa M, Ashida Y, Nishikawa T, Takeda T

机构信息

Department of Senescence Biology, Chest Disease Research Institute, Kyoto University, Japan.

出版信息

Mech Ageing Dev. 1994 May;74(1-2):65-77. doi: 10.1016/0047-6374(94)90099-x.

DOI:10.1016/0047-6374(94)90099-x
PMID:7934209
Abstract

Fibroblast-like cells were isolated from the senescence accelerated mouse (SAM) and cultured, after which evidence of accelerated senescence was sought. Fibroblast-like cell lines were established from the dorsal dermis of neonate mice of both the accelerated senescence-prone strain, SAMP11 and the accelerated senescence-resistant strain, SAMR1. All cell lines from both strains showed a crisis in growth and were immortalized. At crisis, all cultures were composed of morphologically characteristic senescent cells. However, in cell lines from SAMP11, this change was more rapid and at earlier population doublings (PDs) than seen in cell lines from SAMR1. Crises (SAMP11; SAMR1) were also operationally taken to be the point of the least change in PDs (11.2 +/- 1.1; 15.4 +/- 0.5 PDs), the least saturation density (11.3 +/- 0.8; 19.1 +/- 2.6 PDs), and the longest population doubling time (10.1 +/- 0.8; 14.2 +/- 0.6 PDs). Crisis occurred significantly earlier (P < 0.05) and the aging process was accelerated in cell lines from SAMP11, compared with lines from SAMR1. This evidence tends to support various observations made in the accelerated senescence-prone strains of SAMP, in vivo.

摘要

相似文献

1
Accelerated aging of dermal fibroblast-like cells from senescence-accelerated mouse (SAM). 1. Acceleration of population aging in vitro.
Mech Ageing Dev. 1994 May;74(1-2):65-77. doi: 10.1016/0047-6374(94)90099-x.
2
In vitro study of the mechanisms of senescence acceleration.
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3
Accelerated aging of dermal fibroblast-like cells from the senescence-accelerated mouse (SAM): acceleration of changes in DNA ploidy associated with in vitro cellular aging.来自衰老加速小鼠(SAM)的真皮成纤维细胞样细胞的加速衰老:与体外细胞衰老相关的DNA倍性变化加速。
J Gerontol A Biol Sci Med Sci. 1998 Jan;53(1):B11-7. doi: 10.1093/gerona/53a.1.b11.
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Aminoguanidine supplementation delays the onset of senescence in vitro in dermal fibroblast-like cells from senescence-accelerated mice.
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Senescence-accelerated mouse (SAM): a novel murine model of senescence.衰老加速小鼠(SAM):一种新型的衰老小鼠模型。
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[Senescence-accelerated mouse (SAM): with special reference to age-associated pathologies and their modulation].[衰老加速小鼠(SAM):特别提及与年龄相关的病理学及其调节]
Nihon Eiseigaku Zasshi. 1996 Jul;51(2):569-78. doi: 10.1265/jjh.51.569.
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Effects of aging and blood pressure on the structure of the thoracic aorta in SAM mice: a model of age-associated degenerative vascular changes.衰老和血压对SAM小鼠胸主动脉结构的影响:一种与年龄相关的退行性血管变化模型
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Cultured murine dermal fibroblast-like cells from senescence-accelerated mice as in vitro models for higher oxidative stress due to mitochondrial alterations.来自衰老加速小鼠的培养鼠真皮成纤维细胞样细胞作为线粒体改变导致更高氧化应激的体外模型。
J Gerontol A Biol Sci Med Sci. 2005 Sep;60(9):1087-98. doi: 10.1093/gerona/60.9.1087.
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[Proliferative senescence of embryo fibroblasts of Japanese senescence accelerated mice (SAM) is accompanied by parallel decreasing of response to various growth factors].日本快速老化小鼠(SAM)胚胎成纤维细胞的增殖性衰老伴随着对各种生长因子反应的平行下降。
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A higher oxidative status accelerates senescence and aggravates age-dependent disorders in SAMP strains of mice.较高的氧化状态会加速衰老,并加重小鼠SAMP品系中与年龄相关的疾病。
Mech Ageing Dev. 2002 Nov;123(12):1553-61. doi: 10.1016/s0047-6374(02)00091-x.

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