کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6278244 | 1295802 | 2008 | 18 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Morphological and biochemical signs of age-related neurodegenerative changes in klotho mutant mice
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کلمات کلیدی
PBSLC3GFAPTBSHRPMAPK - MAPKAstrocyte - آستروسیتTris-buffered saline - تریس بافر شورsAMP - سمپدوریاLysosome - لیزوزومCSF - مایع مغزی نخاعیCerebrospinal fluid - مایع مغزی نخاعیPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریmap - نقشهneurofilament - نوروفیلامنتSynapse - همایه یا سیناپسHorseradish peroxidase - پراکسیداز هوررادیشGlial fibrillary acidic protein - پروتئین اسیدی فیبریلاسیون گلایالmicrotubule-associated protein - پروتئین مرتبط با میکروتوبولmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenCytoskeleton - چارچوب یاخته، سیتواسکلتون، اسکلت سلولی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Morphological and biochemical signs of age-related neurodegenerative changes in klotho mutant mice Morphological and biochemical signs of age-related neurodegenerative changes in klotho mutant mice](/preview/png/6278244.png)
چکیده انگلیسی
Klotho mutant mice, defective in the klotho gene, develop multiple age-related disorders with very short lifespans. Introduction of the exogenous klotho gene into these mutant mice leads to an improvement in their phenotypes, while overexpression of this gene in wild-type mice significantly extends their lifespan. These observations suggest that the klotho gene/protein has an anti-aging function. Since there have been only a few reports with some disagreement about results on the CNS of the mutant mice, we tried to clarify whether the CNS neurons generate aging-like features, even in premature stages, using biochemical and morphological approaches. Results obtained from the mutant mice, when compared with wild-type mice, were as follows. Neurofilaments (NFs) were increased significantly in axons, with the subunit proteins showing a significant enhancement in phosphorylation or expression of NF-H or NF-L, respectively. Microtubules in Purkinje cell dendrites were closer to each other, and in the CNS tissue tubulin was unaltered, but microtubule-associated protein (MAP) 2 was significantly reduced in expression. Neuronal cellular organelles were morphologically disordered. Lysosomes, cathepsin D and light chain 3 of MAP1A/B (LC3) were augmented with the appearance of putative autophagy-related structures. Antiapoptotic Bcl-xL and proapoptotic Bax were reduced and enhanced, respectively, and mitogen-activated protein kinase was reduced. Synapse-related proteins and structures were decreased. Neuronal degeneration was evident in hippocampal pyramidal cells, and possibly in Purkinje cells. Astrocytic glial filaments and glial fibrillary acidic protein were increased in density and expression, respectively. Together, the CNS neuronal alterations in klotho mutant mice were quite similar to those found in aged animals, including even premature death, so this mouse should be a more appropriate animal model for CNS aging than those previously reported.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 152, Issue 4, 9 April 2008, Pages 924-941
Journal: Neuroscience - Volume 152, Issue 4, 9 April 2008, Pages 924-941
نویسندگان
M. Shiozaki, K. Yoshimura, M. Shibata, M. Koike, N. Matsuura, Y. Uchiyama, T. Gotow,