کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5916804 | 1163756 | 2014 | 14 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
New insights into disease-specific absence of complement factor H related protein C in mouse models of spontaneous autoimmune diseases
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کلمات کلیدی
CFHRBasal laminar depositsBLDDAScollagen antibody-induced arthritisAMDDDDCIICAIACFHcollagen-induced arthritis - آرتروز ناشی از کلاژنRheumatoid arthritis - آرتریتروماتوئیدdense deposit disease - بیماری سپرده متراکمComplement factor H - تکمیل عامل HMacular degeneration - دژنراسیون ماکولاDiabetes mellitus - دیابت قندیSystemic lupus erythematosus - لوپوس اریتماتوی سیستمیکSLE - لوپوس منتشر یا لوپوس اریتماتوس سیستمیکalternative pathway - مسیر جایگزینlectin pathway - مسیر لکتینclassical pathway - مسیر کلاسیکDisease activity score - نمره فعالیت بیماریmembrane attack complex - پیچیده حمله غشاءType II collagen - کلاژن نوع II
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی مولکولی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: New insights into disease-specific absence of complement factor H related protein C in mouse models of spontaneous autoimmune diseases New insights into disease-specific absence of complement factor H related protein C in mouse models of spontaneous autoimmune diseases](/preview/png/5916804.png)
چکیده انگلیسی
Complement factor H (CFH) protein is an inhibitor of the alternative pathway of complement (AP) both in the fluid phase and on the surface of host cells. Mouse and human complement factor H-related (CFHR) proteins also belong to the fH family of plasma glycoproteins. The main goal of the current study was to compare the presence of mRNA for two mCFHR proteins in spontaneously developing autoimmune diseases in mice such as dense deposit disease (DDD), diabetes mellitus (DM), basal laminar deposits (BLD), collagen antibody-induced arthrits (CAIA) and systemic lupus erythematosus (SLE). Here we report for the first time that the CFHR-C mRNA was universally absent in the liver from three strains of lupus-prone mice and in a diabetic-prone mouse strain. The mRNA levels (pg/ng) for CFH and CFHR-B in MRL-lpr/lpr, at 9 wks and 23 wks were 707.2 ± 44.4, 54.5 ± 5.75 and 729 ± 252.9, 74.04 ± 22.76, respectively. The mRNA levels for CFH and CFHR-B in NZB/NZW mice, at 9 wks and 54 wks were 579.9 ± 23.8, 58.8 ± 1.41 and 890.3 ± 135.2, 63.30 ± 9.2, respectively. CFHR-C protein was absent in the circulation of MRL-lpr/lpr and NZB/NZW mice before and after the development of lupus. Similarly, mRNA and protein for CFHR-C was universally absent in liver and other organs and in the circulation of NOD mice before and after the development of DM. In contrast, the mRNAs for CFH, CFHR-B and CFHR-C were universally present in the liver from mice with and without DDD, BLD and CAIA. The levels of mRNA for CFHR-B in mice with and without BLD were â¼4 times higher than the mice with lupus. The complete absence of mRNA for CFHR-C in lupus and diabetic-prone strains indicates that polymorphic variation within the mouse CFHR family exists and raises the possibility that such variation contributes to lupus and diabetic phenotypes.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Immunology - Volume 62, Issue 1, November 2014, Pages 235-248
Journal: Molecular Immunology - Volume 62, Issue 1, November 2014, Pages 235-248
نویسندگان
Gaurav Mehta, Viviana P. Ferreira, Christine Skerka, Peter F. Zipfel, Nirmal K. Banda,