کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10940958 | 1095536 | 2014 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Carboxypeptidase N-deficient mice present with polymorphic disease phenotypes on induction of experimental autoimmune encephalomyelitis
ترجمه فارسی عنوان
موش های کمبود کربوکسی پپتیداز با فنوتیپ های بیماری های پلی مورفیک مبتلا به القاء آنسفالومیلیت های اتوایمیون تجربی
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
MOGEAECPNCVFCarboxypeptidaseMS/EAEexperimental autoimmune encephalomyelitis - آنسفالومیلیت خودایمنی تجربیDemyelinating disease - بیماری دامییلینCobra venom factor - عامل سم کبراcarboxypeptidase N - کربوکسی پپتیداز NKinins - کینینزmyelin oligodendrocyte glycoprotein - گلیکوپروتئین الیگودندروسیت میلین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
چکیده انگلیسی
Carboxypeptidase N (CPN) is a member of the carboxypeptidase family of enzymes that cleave carboxy-terminal lysine and arginine residues from a large number of biologically active peptides and proteins. These enzymes are best known for their roles in modulating the activity of kinins, complement anaphylatoxins and coagulation proteins. Although CPN makes important contributions to acute inflammatory events, little is known about its role in autoimmune disease. In this study we used CPNâ/â mice in experimental autoimmune encephalomyelitis (EAE), the animal model for multiple sclerosis. Unexpectedly, we observed several EAE disease phenotypes in CPNâ/â mice compared to wild type mice. The majority of CPNâ/â mice died within five to seven days after disease induction, before displaying clinical signs of disease. The remaining mice presented with either mild EAE or did not develop EAE. In addition, CPNâ/â mice injected with complete or incomplete Freund's adjuvant died within the same time frame and in similar numbers as those induced for EAE. Overall, the course of EAE in CPNâ/â mice was significantly delayed and attenuated compared to wild type mice. Spinal cord histopathology in CPNâ/â mice revealed meningeal, but not parenchymal leukocyte infiltration, and minimal demyelination. Our results indicate that CPN plays an important role in EAE development and progression and suggests that multiple CPN ligands contribute to the disease phenotypes we observed.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Immunobiology - Volume 219, Issue 2, February 2014, Pages 104-108
Journal: Immunobiology - Volume 219, Issue 2, February 2014, Pages 104-108
نویسندگان
Xianzhen Hu, Rick A. Wetsel, Theresa N. Ramos, Stacey L. Mueller-Ortiz, Trenton R. Schoeb, Scott R. Barnum,