کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6272466 | 1614781 | 2015 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Forebrain neuronal specific ablation of p53 gene provides protection in a cortical ischemic stroke model
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کلمات کلیدی
MCAPFATBIBSA - BSATraumatic brain injury - آسیب تروماتیک مغزbovine serum albumin - آلبومین سرم گاوphosphate buffer - بافر فسفاتanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of varianceStroke - سکته مغزیmiddle cerebral artery - شریان مغزی میانیNeuroprotection - محافظت نورونی یا محافظت از عصبknockout - ناکاوتwildtype - نوع وحشیparaformaldehyde - پارافرمالدهید
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
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چکیده انگلیسی
Cerebral ischemic injury involves death of multiple cell types at the ischemic sites. As a key regulator of cell death, the p53 gene has been implicated in the regulation of cell loss in stroke. Less focal damage is found in stroke animals pre-treated with a p53 inhibitor or in traditional p53 knockout (ko) mice. However, whether the p53 gene plays a direct role in regulating neuronal cell death is unknown. In this study, in contrast to the global inhibition of p53 function by pharmacological inhibitors and in traditional p53 ko mice, we utilized a neuronal specific conditional ko mouse line (CamcreTRP53Â loxP/loxP) to achieve forebrain neuronal specific deletion of p53 and examined the role of the p53 gene in ischemia-induced cell death in neurons. Expression of p53 after stroke is examined using the immunohistochemical method and the outcome of stroke is examined by analysis of infarction size and behavioral deficits caused by stroke. Our data showed that p53 expression is upregulated in the ischemic region in neuronal cells in wildtype (wt) mice but not in CamcreTRP53Â loxP/loxP ko mice. Deletion of the p53 gene in forebrain neurons results in a decreased infarction area in ko mice. Locomotor behavior, measured in automated activity chambers, showed that CamcreTRP53Â loxP/loxP ko mice have less locomotor deficits compared to wt mice after middle cerebral artery occlusion (MCAo). We conclude that manipulation of p53 expression in neurons may lead to unique therapeutic development in stroke.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 295, 4 June 2015, Pages 1-10
Journal: Neuroscience - Volume 295, 4 June 2015, Pages 1-10
نویسندگان
E. Filichia, H. Shen, X. Zhou, X. Qi, K. Jin, N. Greig, B. Hoffer, Y. Luo,