کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2899306 1173130 2006 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Pulmonary vein stenosis: expression of receptor tyrosine kinases by lesional cells
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی کاردیولوژی و پزشکی قلب و عروق
پیش نمایش صفحه اول مقاله
Pulmonary vein stenosis: expression of receptor tyrosine kinases by lesional cells
چکیده انگلیسی

BackgroundPrimary pulmonary vein stenosis (PVS) is a progressive disorder of infants. Although catheter based intervention and chemotherapy are used to manage the disorder, the benefit of these approaches is reduced considerably by restenosis. The nature of the intimal cells causing the occlusive lesions in PVS is poorly understood.MethodsSeven PVS cases were studied with antibodies for smooth muscle actin (SMA), muscle-specific actin (MSA), monoclonal desmin, S100 protein, CD31, CD34, CD45RO, CD68, CD99, Ki-67 (MIB-I), and with antibodies directed against several receptor tyrosine kinases (RTK), including platelet-derived growth factor alpha and beta receptor (PDGFR-α and -β), epidermal growth factor receptor (EGFR), fibroblast growth factor receptor (FGFR), vascular endothelial growth factor 1 and 2 receptor (VEGFR), and stem cell factor receptor (c-kit).ResultsLesional cells stained strongly and diffusely with SMA and MSA, but not for macrophage, lymphocyte, endothelial markers, or for Ki-67. RTK expression was strong and diffuse for PDGFR-α and -β, FGFR, and VEGFR-2. Lesional cells stained for VEGF and PDGF β receptor was phosphorylated.ConclusionsThe histologic appearance, and the strong diffuse immunoreactivity for smooth muscle markers, indicates that the intimal lesional cells are myofibroblast-like. Expression of various receptor tyrosine kinases and some ligands suggests an autocrine or paracrine role of these proteins in the pathogenesis of the intimal occlusive lesion in PVS.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cardiovascular Pathology - Volume 15, Issue 2, March–April 2006, Pages 91–99
نویسندگان
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