کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6273400 | 1614797 | 2014 | 16 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Photoreceptor degeneration, structural remodeling and glial activation: A morphological study on a genetic mouse model for pericyte deficiency
ترجمه فارسی عنوان
دژنراسیون فتوگرامتر، بازسازی ساختاری و فعال سازی گلیال: یک مطالعه ی مورفولوژیکی بر روی مدل موش های ژنتیکی برای کمبود پرسیت
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کلمات کلیدی
PDGFR-βNG2α-SMAONLINLIBA1IB4RPEOPLTSPOPDGF-BPKCαPNAGFAPPlatelet-derived growth factor BPBSBSA - BSAbovine serum albumin - آلبومین سرم گاوalpha smooth muscle actin - آلفا آکتیو عضله صافneuron-glial antigen 2 - آنتی ژن نئون گلیال 2peanut agglutinin - آگلوتینین بادام زمینیretinal pigment epithelium - اپیتلیوم رنگدانه شبکیهisolectin B4 - ایزوکتین B4Cho - برایTerminal deoxynucleotidyl transferase dUTP nick end labeling - ترمینال deoxynucleotidyl transferase dUTP نام نهایی پایان نامهTUNEL - تونلPhotoreceptor degeneration - دژنراسیون فتوترپتورRho - روRhodopsin - رودوپسینpostnatal day - روز پس از زایمانRosette - روزتMüller cells - سلول های مولرOptic nerve - عصب بیناییouter plexiform layer - لایه بیرونی بیرونیouter nuclear layer - لایه بیرونی هسته ایinner nuclear layer - لایه داخلی هسته ایPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریCell death - مرگ سلولی ionized calcium binding adapter molecule 1 - مولکول آداپتور اتصال دهنده کلسیم یونیزه 1Microglia - میکروگلیاهاSynapse - همایه یا سیناپسGlial fibrillary acidic protein - پروتئین اسیدی فیبریلاسیون گلایالtranslocator protein - پروتئین ترجمه شدهprotein kinase C alpha - پروتئین کیناز C آلفاplatelet-derived growth factor receptor beta - پلاکت عامل گیرنده بتای فاکتور رشدcleaved caspase-3 - کاسیاس شکسته 3Choroid - کوروید
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
چکیده انگلیسی
Interaction between pericytes and endothelial cells via platelet-derived growth factor B (PDGF-B) signaling is critical for the development of the retinal microvasculature. The PDGF-B retention motif controls the spatial distribution range of the growth factor in the vicinity of its producing endothelial cells allowing its recognition by PDGF receptor beta-(PDGFR-β)-carrying pericytes; this promotes recruitment of pericytes to the vascular basement membrane. Impairment of the PDGF-B signaling mechanism causes development of vascular abnormalities, and in the retina this consequently leads to defects in the neurological circuitry. The vascular pathology in the pdgf-bret/ret (PDGF-B retention motif knockout) mouse retina has been previously reported; our study investigates the progressive neuronal defects and changes in the retinal morphology of this pericyte-deficient mouse model. Immunohistochemical analysis revealed retinal injuries to occur as early as postnatal day (P) 10 with substantial damage progressing from P15 and onward. Vascular abnormalities were apparent from P10, however, prominent neuronal defects were mostly observed from P15, beginning with the compromised integrity of the laminated retinal structure characterized by the presence of rosettes and focally distorted regions. Photoreceptor degeneration was observed by loss of both rod and cone cells, including the disassembly and altered structure of their synaptic terminals. Significant shortening of cone outer segments was observed from P10 and later stages; however, decrease in cone density was only observed at P28. Disorganization and dendrite remodeling of rod bipolar cells also added to the diminished neural and synaptic integrity. Moreover, in response to retinal injuries, Müller and microglial cells were observed to be in the reactive phenotype from P15 and onward. Such a sequence of events indicates that the pdgf-bret/ret mouse model displays a short time frame between P10 and P15, during which the retina shifts to a retinopathic phase by the development of prominently altered morphological features.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 279, 24 October 2014, Pages 269-284
Journal: Neuroscience - Volume 279, 24 October 2014, Pages 269-284
نویسندگان
G. Genové, T. Mollick, K. Johansson,