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Tytuł pozycji:

The Novel Pathogenesis of Retinopathy Mediated by Multiple RTK Signals is Uncovered in Newly Developed Mouse Model.

Tytuł :
The Novel Pathogenesis of Retinopathy Mediated by Multiple RTK Signals is Uncovered in Newly Developed Mouse Model.
Autorzy :
Kitahara H; Department of Pathology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama-shi, Toyama 930-0194, Japan; Department of Japanese Oriental Medicine, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama-shi, Toyama 930-0194, Japan.
Kajikawa S; Department of Pathology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama-shi, Toyama 930-0194, Japan.
Ishii Y; Department of Pathology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama-shi, Toyama 930-0194, Japan.
Yamamoto S; Department of Pathology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama-shi, Toyama 930-0194, Japan. Electronic address: .
Hamashima T; Department of Pathology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama-shi, Toyama 930-0194, Japan.
Azuma E; Department of Pathology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama-shi, Toyama 930-0194, Japan; Department of Technology Development, Toyama Technology Center, Astellas Pharma Tech Co., Ltd., 2-178 Kojin-machi, Toyama-shi, Toyama 930-0809, Japan.
Sato H; Department of Neurosurgery, Tokyo General Hospital, 3-15-2 Egota, Nakano-ku, Tokyo 165-0022, Japan.
Matsushima T; Department of Pathology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama-shi, Toyama 930-0194, Japan.
Shibuya M; Department of Research and Education, Jobu University, 634-1 Toyazuka-machi, Isesaki-shi, Gunma 372-8588, Japan.
Shimada Y; Department of Japanese Oriental Medicine, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama-shi, Toyama 930-0194, Japan.
Sasahara M; Department of Pathology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama-shi, Toyama 930-0194, Japan. Electronic address: .
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Źródło :
EBioMedicine [EBioMedicine] 2018 May; Vol. 31, pp. 190-201. Date of Electronic Publication: 2018 Apr 25.
Typ publikacji :
Journal Article
Język :
English
Imprint Name(s) :
Original Publication: [Amsterdam] : Elsevier B.V., [2014]-
MeSH Terms :
Diabetic Retinopathy*/genetics
Diabetic Retinopathy*/metabolism
Diabetic Retinopathy*/pathology
Eye Proteins*/genetics
Eye Proteins*/metabolism
Pericytes*/metabolism
Pericytes*/pathology
Retina*/metabolism
Retina*/pathology
Signal Transduction*
Animals ; Becaplermin ; Disease Models, Animal ; Membrane Proteins ; Mice ; Mice, Knockout ; Proteins/genetics ; Proteins/metabolism ; Proto-Oncogene Proteins c-sis/genetics ; Proto-Oncogene Proteins c-sis/metabolism ; Receptor, Platelet-Derived Growth Factor beta/genetics ; Receptor, Platelet-Derived Growth Factor beta/metabolism ; Vascular Endothelial Growth Factor A/genetics ; Vascular Endothelial Growth Factor A/metabolism ; Vascular Endothelial Growth Factor Receptor-1/genetics ; Vascular Endothelial Growth Factor Receptor-1/metabolism
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Contributed Indexing :
Keywords: PDGF; Pathological angiogenesis; PlGF; Proliferative membrane; Retinopathy; VEGF
Substance Nomenclature :
0 (Eye Proteins)
0 (Membrane Proteins)
0 (Pigf protein, mouse)
0 (Proteins)
0 (Proto-Oncogene Proteins c-sis)
0 (Vascular Endothelial Growth Factor A)
0 (vascular endothelial growth factor A, mouse)
1B56C968OA (Becaplermin)
EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor beta)
EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-1)
Entry Date(s) :
Date Created: 20180505 Date Completed: 20180924 Latest Revision: 20210109
Update Code :
20210110
PubMed Central ID :
PMC6013936
DOI :
10.1016/j.ebiom.2018.04.021
PMID :
29724654
Czasopismo naukowe
Pericyte desorption from retinal blood vessels and subsequent vascular abnormalities are the pathogenesis of diabetic retinopathy (DR). Although the involvement of abnormal signals including platelet-derived growth factor receptor-β (PDGFRβ) and vascular endothelial growth factor-A (VEGF-A) have been hypothesized in DR, the mechanisms that underlie this processes are largely unknown. Here, novel retinopathy mouse model (N-PRβ-KO) was developed with conditional Pdgfrb gene deletion by Nestin promoter-driven Cre recombinase (Nestin-Cre) that consistently reproduced through early non-proliferative to late proliferative DR pathologies. Depletion of Nestin-Cre-sensitive PDGFRβ + NG2 + αSMA - pericytes suppressed pericyte-coverages and induced severe vascular lesion and hemorrhage. Nestin-Cre-insensitive PDGFRβ + NG2 + αSMA + pericytes detached from the vascular wall, and subsequently changed into myofibroblasts in proliferative membrane to cause retinal traction. PDGFRα + astrogliosis was seen in degenerated retina. Expressions of placental growth factor (PlGF), VEGF-A and PDGF-BB were significantly increased in the retina of N-PRβ-KO. PDGF-BB may contribute to the pericyte-fibroblast transition and glial scar formation. Since VEGFR1 signal blockade significantly ameliorated the vascular phenotype in N-PRβ-KO mice, the augmented VEGFR1 signal by PlGF and VEGF-A was indicated to mediate vascular lesions. In addition to PDGF-BB, PlGF and VEGF-A with their intracellular signals may be the relevant therapeutic targets to protect eyes from DR.
(Copyright © 2018 The Authors. Published by Elsevier B.V. All rights reserved.)

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