کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6270999 | 1614750 | 2016 | 49 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
β-Dystroglycan cleavage by matrix metalloproteinase-2/-9 disturbs aquaporin-4 polarization and influences brain edema in acute cerebral ischemia
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کلمات کلیدی
Transient MCAOMMPTMCAOpMCAOICAAquaporin-4AQP4DGCβ-dystroglycan - β-دیستروگلیکانAngiotensin II - آنژیوتانسین دوBrain edema - ادم مغزیPermanent middle cerebral artery occlusion - انسداد شریان مغزی میانی دائمیCerebral ischemia - ایسکمی مغزیanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of varianceAng II - دومDystroglycan - دیستروگلیکانBlood–brain barrier - سد خونی مغزیBBB - سد خونی مغزیinternal carotid artery - شریان کاروتید داخلیbasement membrane - غشای پایهBlood pressure - فشارخونmatrix metalloproteinase - ماتریکس متالوپروتئینازMatrix metalloproteinase-9 - ماتریکس متالوپروتئیناز -9Matrix metalloproteinase-2 - ماتریکس متالوپروتئیناز-2hematoxylin–eosin - هماتوکسیلین ائوزینpolymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمرازDystrophin glycoprotein complex - پیچیده گلیکوپروتئین دیستروفین
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Dystroglycan (DG) is widely expressed in various tissues, and throughout the cerebral microvasculature. It consists of two subunits, α-DG and β-DG, and the cleavage of the latter by matrix metalloproteinase (MMP)-2 and -9 underlies a number of physiological and pathological processes. However, the involvement of MMP-2/-9-mediated β-DG cleavage in cerebral ischemia remains uncertain. In astrocytes, DG is crucial for maintaining the polarization of aquaporin-4 (AQP4), which plays a role in the regulation of cytotoxic and vasogenic edema. The present study aimed to explore the effects of MMP-2/-9-mediated β-DG cleavage on AQP4 polarization and brain edema in acute cerebral ischemia. A model of cerebral ischemia was established via permanent middle cerebral artery occlusion (pMCAO) in male C57BL/6 mice. Western blotting, real-time polymerase chain reaction (PCR), immunohistochemical staining, immunofluorescent staining, electron microscopy, and light microscopy were used. Captopril was applied as a selective MMP-2/-9 inhibitor. Recombinant mouse MMP (rmMMP)-2 and -9 were used in an in vitro cleavage experiment. The present study demonstrated evidence of β-DG cleavage by MMP-2/-9 in pMCAO mouse brains; this cleavage was implicated in AQP4 redistribution and brain edema in cerebral ischemia. In addition, captopril exacerbated cytotoxic edema and ameliorated vasogenic edema at 24 h after pMCAO, and alleviated brain edema and neurological deficit at 48 h and 72 h. In conclusion, this study provides novel insight into the effects of MMP-2/-9-mediated β-DG cleavage in acute cerebral ischemia. Such findings might facilitate the development of a therapeutic strategy for the optimization of MMP-2/-9 targeted treatment in cerebral ischemia.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 326, 21 June 2016, Pages 141-157
Journal: Neuroscience - Volume 326, 21 June 2016, Pages 141-157
نویسندگان
W. Yan, X. Zhao, H. Chen, D. Zhong, J. Jin, Q. Qin, H. Zhang, S. Ma, G. Li,