کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4330249 | 1614254 | 2007 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Poxvirus-derived cytokine response modifier A (CrmA) does not protect against focal cerebral ischemia in mice
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کلمات کلیدی
DAPITNF receptor familyTdTLDFPFAABCSSCNGSFITCMCAPBSstandard deviation - انحراف معیارterminal deoxynucleotidyl transferase - ترمینال deoxynucleotidyl transferaseTUNEL - تونلlaser Doppler flow - جریان داپلر لیزرnormal goat serum - سرم طبیعی بزIschemic stroke - سکته مغزی ایسکمیکmiddle cerebral artery - شریان مغزی میانیfluorescein isothiocyanate - فلوئورسین ایسوتیوسیاناتPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریApoptotic cell death - مرگ سلولی آپوپتوزCaspase inhibitor - مهار کننده کاسپازpolymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمرازparaformaldehyde - پارافرمالدهید
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
In ischemic stroke, cytosolic death pathways are activated in injured neurons destined to die. Neuronal injury is modulated by cell surface receptors, among which the tumor necrosis factor receptor family obtained particular interest. Cytokine response modifier A (CrmA) is a cowpox virus-derived caspase inhibitor, which interferes with the so-called death-inducing signaling complex, thereby blocking receptor-mediated apoptosis. To elucidate CrmA's therapeutic potential in ischemic stroke, we characterized a transgenic mouse line expressing CrmA under a Thy1 promoter, which we subjected to intraluminal middle cerebral artery (MCA) occlusion. Using in situ hybridization histochemistry and Western blots, we show that the crmA gene integrated into chromosome 8 of the mouse genome, CrmA being expressed in the cerebral cortex and striatum. Although robustly expressed, transgenic CrmA did not influence ischemic injury, both when relatively long-lasting (90Â min) and mild (30Â min) MCA occlusions were imposed. As such, neither infarct volume, brain swelling or neurological deficits following 90-min ischemia, nor disseminated neuronal injury or caspase-3 activation following 30-min ischemia were influenced by CrmA. Our data argue against a therapeutic effect of CrmA in ischemic stroke.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1185, 14 December 2007, Pages 293-300
Journal: Brain Research - Volume 1185, 14 December 2007, Pages 293-300
نویسندگان
Ertugrul Kilic, Andreas Wippel, Ãlkan Kilic, Peter Vogel, Mia Kim, Herman van der Putten, Christoph Wiessner, Giorgio Rovelli, Bernd W. Böttiger, Dirk M. Hermann,