کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5887981 | 1152298 | 2016 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Dermal lymphatic dilation in a mouse model of alopecia areata
ترجمه فارسی عنوان
التهاب لنفاوی پوستی در یک مدل موی آلوپسی آرئاتا
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کلمات کلیدی
FMS-like tyrosine kinase 1LymphaticsCXCR4CCR7PodoplaninFLT1CXCL11alopecia areataKDRchemokine (C-X-C motif) ligand 12PDPNLYVE1PECAM1H&E - H & Einflammation - التهاب( توروم) endothelin 1 - اندوتلین 1Autoimmune disease - بیماری خودایمنیSMA - دبیرستانhematoxylin and eosin stain - رنگ آمیزی هماتوکسیلین و ائوزینlymphatic vessel endothelial hyaluronan receptor 1 - گیرنده هیالورونان اندوتلیال عروق لنفاوی 1
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیوشیمی بالینی
چکیده انگلیسی
Mouse models of various types of inflammatory skin disease are often accompanied by increased dermal angiogenesis. The C3H/HeJ inbred strain spontaneously develops alopecia areata (AA), a cell mediated autoimmune disorder that can be controllably expanded using full thickness skin grafts to young unaffected mice. This provides a reproducible and progressive model for AA in which the vascularization of the skin can be examined. Mice receiving skin grafts from AA or normal mice were evaluated at 5, 10, 15, and 20Â weeks after engraftment. Lymphatics are often overlooked as they are small slit-like structures above the hair follicle that resemble artifact-like separation of collagen bundles with some fixatives. Lymphatics are easily detected using lymphatic vessel endothelial hyaluronan receptor 1 (LYVE1) by immunohistochemistry to label their endothelial cells. Using LYVE1, there were no changes in distribution or numbers of lymphatics although they were more prominent (dilated) in the mice with AA. Lyve1 transcripts were not significantly upregulated except at 10Â weeks after skin grafting when clinical signs of AA first become apparent. Other genes involved with vascular growth and dilation or movement of immune cells were dysregulated, mostly upregulated. These findings emphasize aspects of AA not commonly considered and provide potential targets for therapeutic intervention.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental and Molecular Pathology - Volume 100, Issue 2, April 2016, Pages 332-336
Journal: Experimental and Molecular Pathology - Volume 100, Issue 2, April 2016, Pages 332-336
نویسندگان
John P. Sundberg, C. Herbert Pratt, Kathleen A. Silva, Victoria E. Kennedy, Timothy M. Stearns, Beth A. Sundberg, Lloyd E. King, Harm HogenEsch,