کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6278666 | 1295855 | 2007 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Correlative association between circadian expression of mousePer2 gene and the proliferation of the neural stem cells
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کلمات کلیدی
EGFPBSmPer2MPEROligonucleotidesBrdU incorporationODNs - ODN هاBrdU - بروموداکسی اوریدینbromodeoxyuridine - برومودسوویریدینProliferation - ترویجper - در هرPeriod - دوره زمانیcircadian - دیروزNeural stem cell - سلول های بنیادی عصبیepidermal growth factor - عامل رشد اپیدرمیPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافری
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
We examined the circadian expression of mousePeriod (mPer) genes (mPer1 and mPer2) and the proliferation of the neural stem cells in vitro. The neural stem cells from the ganglionic eminence of embryonic mice were expanded by the neurosphere method and then treated with epidermal growth factor (EGF) to stimulate their mitotic activity. The time courses of the proliferation were examined by WST-8 assay and bromodeoxyuridine (BrdU) incorporation assay and the expression of mPer1 and mPer2 genes was examined by RT-PCR and immunocytochemistry. We have found that EGF treatment elicited the circadian change in both the increase in viable cell number and DNA synthesis activity of the neural stem cells. Also, the gene expression of mPer2, but not mPer1, changed rhythmically with a period of 24 h and correlated negatively with the DNA synthesis activity rhythm. Furthermore, the treatment with an antisense oligonucleotide against mPer2 increased the DNA synthesis activity of the neural stem cells. These results suggest that mPer2 might periodically suppress the proliferation of neural stem cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 146, Issue 2, 11 May 2007, Pages 494-498
Journal: Neuroscience - Volume 146, Issue 2, 11 May 2007, Pages 494-498
نویسندگان
T. Moriya, K. Hiraishi, N. Horie, M. Mitome, K. Shinohara,