کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6022224 | 1580666 | 2013 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Modulation of neural stem/progenitor cell proliferation during experimental Herpes Simplex encephalitis is mediated by differential FGF-2 expression in the adult brain
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Modulation of neural stem/progenitor cell proliferation during experimental Herpes Simplex encephalitis is mediated by differential FGF-2 expression in the adult brain Modulation of neural stem/progenitor cell proliferation during experimental Herpes Simplex encephalitis is mediated by differential FGF-2 expression in the adult brain](/preview/png/6022224.png)
چکیده انگلیسی
Neural stem cells (NSCs) respond to inflammatory cues induced during brain injury and are thought to be involved in recovery from brain damage. Little is known about NSC response during brain infections. The present study evaluated NSC proliferation during Herpes Simplex Virus-1 brain infection. Total numbers of nestin(+) NSCs increased significantly in infected brains at 6Â days post infection (p.i.). However, by 15Â days p.i. the nestin(+) population decreased significantly below levels observed in uninfected brains and remained depressed through 30Â days p.i. This initial increase in NSC population occurred concurrently with increased brain cell proliferation, which peaked at 3Â days p.i. On closer examination, we found that while actively proliferating Sox2(+) NSCs increased in number at 6Â days p.i., proliferating DCX(+) neuroblasts contributed to the increased response at 3Â days p.i. However, overall proliferation decreased steadily from 15Â days p.i. to below control levels. To determine the mechanisms involved in altering NSC proliferation, neurotrophin and growth factor expression profiles were assessed. FGF-2 gene expression increased at 5Â days p.i. and was robustly down-regulated at 15Â days p.i. (>Â 1000-fold), which was further confirmed by increased FGF-2 immunostaining around the lateral ventricles. Furthermore, supplementing infected animals with recombinant FGF-2, at 15Â days p.i., significantly increased the number of proliferating brain cells. These findings demonstrate that the temporal changes in NSC proliferation are mediated through the regulation of FGF-2 and that the NSC niche may benefit from supplementation with FGF-2 during HSV-1 brain infection.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Disease - Volume 58, October 2013, Pages 144-155
Journal: Neurobiology of Disease - Volume 58, October 2013, Pages 144-155
نویسندگان
Jessica H. Rotschafer, Shuxian Hu, Morgan Little, Melissa Erickson, Walter C. Low, Maxim C.J. Cheeran,