کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6272432 | 1614772 | 2015 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
ETB receptor-mediated MMP-9 activation induces vasogenic edema via ZO-1 protein degradation following status epilepticus
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کلمات کلیدی
PBSDABeNOSGFAPDTTMMP-9TBS3,3′-diaminobenzidine - 3،3'-diaminobenzidineTight junction - اتصال تنگVasogenic edema - ادم واژننیکSprague-Dawley - اسپراگ داولیphosphate buffer - بافر فسفاتstatus epilepticus - بحران صرعی یا صرع پایدارTris-buffered saline - تریس بافر شورdithiothreitol - دیتیوتریتولBBB - سد خونی مغزیBlood–brain barrier - سد خونی مغزیendothelial nitric oxide synthase - سنتاز اکسید نیتریک اندوتلیالzonula occludens - شل بستنOccludin - عذابpiriform cortex - قشر پریکومMatrix metalloproteinase-9 - ماتریکس متالوپروتئیناز -9Phosphate-buffered saline - محلول نمک فسفات با خاصیت بافریZonula occludens-1 - نوار ابزار بسته 1Glial fibrillary acidic protein - پروتئین اسیدی فیبریلاسیون گلایالClaudin-5 - کلودین-5ETB receptor - گیرنده ETBendothelin B receptor - گیرنده اندوتلین B
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
The blood-brain barrier (BBB) is formed by the endothelial cells with specialized tight junctions (TJs) lining the blood vessels and astroglial endfeet surrounding the blood vessels. Although BBB disruption during brain insults leads to vasogenic edema as one of the primary steps in the epileptogenic process, little is known about the molecular and physiological events concerning vasogenic edema formation. In the present study, status epilepticus (SE) changed the expressions and subcellular localizations of TJ proteins (claudin-5, occludin and zonula occludens-1 (ZO-1)) in endothelial cells of the rat piriform cortex. Among TJ proteins, the alteration in ZO-1 expression was relevant to endothelin B (ETB) receptor-mediated endothelial nitric oxide synthase (eNOS) activation, which increased matrix metalloproteinase-9 (MMP-9) activity. Indeed, BQ788 (an ETB receptor antagonist) effectively attenuated SE-induced vasogenic edema by inhibiting eNOS-mediated MMP-9 activation and ZO-1 protein degradation in endothelial cells, although astroglial endfeet were detached from endothelial cells. Therefore, we suggest that SE-induced ETB receptor/eNOS-mediated MMP-9 activation may lead to impairments of endothelial cell function via TJ protein degradation, which are involved in vasogenic edema formation independent of perivascular astroglial functions.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 304, 24 September 2015, Pages 355-367
Journal: Neuroscience - Volume 304, 24 September 2015, Pages 355-367
نویسندگان
J.Y. Kim, A.-R. Ko, H.-W. Hyun, T.-C. Kang,