کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6278251 | 1295802 | 2008 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Epigenetic regulation of the estrogen receptor alpha promoter in the cerebral cortex following ischemia in male and female rats
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کلمات کلیدی
MSPERβERαMecp2MCAOovariectomizedOVXBDNF - BDNF یا فاکتور نورونزایی مشتقشده از مغز Methylation-specific PCR - PCR اختصاصی متیلاتEstrogen - استروژنmiddle cerebral artery occlusion - انسداد شریان (سرخرگ) مغزی میانیchromatin immunoprecipitation - ایمن سازی کروماتینimmunoreactive - ایمنی فعالImmunohistochemistry - ایمونوهیستوشیمیIHC - ایمونوهیستوشیمیStroke - سکته مغزیBrain-derived neurotrophic factor - فاکتور نوروتروفی مشتق شده از مغزMethylation - متیلاسیونmethyl CpG binding protein 2 - پروتئین متصل CpG متیل 2CHiP - چیپEstrogen receptor alpha - گیرنده استروژن آلفاEstrogen receptor beta - گیرنده استروژن بتا
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Permanent middle cerebral artery occlusion (MCAO) causes neuronal cell death in the striatum and cortex. In rodents, estradiol treatment protects the cortex from cell death in an estrogen receptor alpha (ERα) dependent manner. ERα is only transiently expressed in the cortex during neonatal development and is very low in uninjured adult cortex. Following MCAO, ERα mRNA expression is upregulated in the cortex of female rats, but the mechanism of this increase is still unknown. It is also unknown whether a similar increase in ERα expression in seen in males. In the following studies, male and vehicle or estradiol-treated ovariectomized (OVX) female rats underwent MCAO to investigate the regulation of ERα expression after ischemia. Twenty-four hours after surgery, mRNA or genomic DNA was collected from 1 mm micropunches taken from 300 μm brain sections for quantitative reverse transcription-polymerase chain reaction (RT-PCR) or methylation-specific (MSP) PCR, respectively. Additionally, adjacent 20 μm sections were processed for ERα immunohistochemistry. In OVX females, ERα mRNA and protein were increased in the ischemic cortex, but unchanged in males. We hypothesized that this increase in ERα in females is due to a reversal of gene silencing by DNA methylation. Using MSP targeting of CpG islands within the 5â² untranslated region (UTR) of the rat ERα gene, we found that ischemia decreased methylation in the ischemic cortex of both groups of females, but there was no change in methylation in males. Using chromatin immunoprecipitation, we found that MeCP2 associates with ERα 5â²UTR corresponding with the methylation status of the promoter. These data are the first to demonstrate a difference in the regulation of ERα expression in response to MCAO between males and females and that methylation of the ERα gene corresponds with mRNA levels in the brain.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 152, Issue 4, 9 April 2008, Pages 982-989
Journal: Neuroscience - Volume 152, Issue 4, 9 April 2008, Pages 982-989
نویسندگان
J.M. Westberry, A.K. Prewitt, M.E. Wilson,