scholarly journals Origin of the fast negative ERG component from isolated aspartate-treated mouse retina

2009 ◽  
Vol 9 (12) ◽  
pp. 9-9 ◽  
Author(s):  
F. J. Vinberg ◽  
S. Strandman ◽  
A. Koskelainen
Keyword(s):  
Treated Mouse ◽  
Mouse Retina ◽  
Negative Erg

scholarly journals Advanced glycation end products induce immature angiogenesis in in vivo and ex vivo mouse models

2020 ◽  
Vol 318 (3) ◽  
pp. H519-H533 ◽  
Author(s):  
Lixian Chen ◽  
Yun Cui ◽  
Bingyu Li ◽  
Jie Weng ◽  
Weiju Wang ◽  
...  
Keyword(s):  
Diabetic Retinopathy ◽  
Advanced Glycation End Products ◽  
Ex Vivo ◽  
Aortic Ring ◽  
Treated Mouse ◽  
Mouse Retina ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

Proliferative diabetic retinopathy (PDR) is a progressive disease predominantly involving pathological angiogenesis and is characterized by the development of immature, fragile, and easily hemorrhagic new vessels. Advanced glycation end products (AGEs) and the receptor for AGEs (RAGE) play important roles in the progression of diabetic retinopathy. Our previous studies demonstrated that AGEs promoted HUVEC angiogenesis by inducing moesin phosphorylation via RhoA/Rho-associated protein kinase (ROCK) pathway. The aim of this study was to further confirm AGE-induced angiogenesis in vivo and the involvement of RAGE, ROCK, and moesin phosphorylation in this process. We performed the study in an AGE-treated mouse model with various angiogenesis assays in multiple in vivo and ex vivo models. The results demonstrated that AGEs promoted significant neovascularization in whole mount retina and mouse aortic ring of adult and postnatal mice and in Matrigel plug as well, which were consistently accompanied by increased moesin phosphorylation. The increase of AGE-evoked neovascularization and moesin phosphorylation were both attenuated by RAGE knockout or ROCK inhibitor Y27632 administration in mice. We also revealed the pathological characteristics of AGE-promoted angiogenesis by demonstrating the decrease of pericyte coverage and the disarranged endothelial alignment in microvessels. In conclusion, this study provides in vivo evidences that AGEs induce immature angiogenesis by binding to RAGE, activating the RhoA/ROCK signal pathway and inducing moesin phosphorylation. NEW & NOTEWORTHY Advanced glycation end product (AGE)-induced formation of neovessels and phosphorylation of moesin in retina and aortic ring required AGE receptors. AGEs increased neovessels and the phosphorylation of moesin in retina and aortic ring via RhoA/ROCK pathway. AGE-induced immature angiogenesis in AGE-treated mouse retina and aortic ring. The AGE-RAGE axis and moesin could be candidate targets for overcoming relative diseases.

scholarly journals Exacerbation of AMD Phenotype in Lasered CNV Murine Model by Dysbiotic Oral Pathogens

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 309
Author(s):  
Pachiappan Arjunan ◽  
Radhika Swaminathan ◽  
Jessie Yuan ◽  
Mohamed Elashiry ◽  
Amany Tawfik ◽  
...  
Keyword(s):  
Murine Model ◽  
Retinal Thickness ◽  
Age Related Macular Degeneration ◽  
Periodontal Pathogen ◽  
Fundus Photography ◽  
Mouse Retina ◽  
Rrna Gene ◽  
Age Related ◽  
Periodontal Infection

Emerging evidence underscores an association between age-related macular degeneration (AMD) and periodontal disease (PD), yet the biological basis of this linkage and the specific role of oral dysbiosis caused by PD in AMD pathophysiology remains unclear. Furthermore, a simple reproducible model that emulates characteristics of both AMD and PD has been lacking. Hence, we established a novel AMD+PD murine model to decipher the potential role of oral infection (ligature-enhanced) with the keystone periodontal pathogen Porphyromonas gingivalis, in the progression of neovasculogenesis in a laser-induced choroidal-neovascularization (Li-CNV) mouse retina. By a combination of fundus photography, optical coherence tomography, and fluorescein angiography, we documented inflammatory drusen-like lesions, reduced retinal thickness, and increased vascular leakage in AMD+PD mice retinae. H&E further confirmed a significant reduction of retinal thickness and subretinal drusen-like deposits. Immunofluorescence microscopy revealed significant induction of choroidal/retinal vasculogenesis in AMD+PD mice. qPCR identified increased expression of oxidative-stress, angiogenesis, pro-inflammatory mediators, whereas antioxidants and anti-inflammatory genes in AMD+PD mice retinae were notably decreased. Through qPCR, we detected Pg and its fimbrial 16s-RrNA gene expression in the AMD+PD mice retinae. To sum-up, this is the first in vivo study signifying a role of periodontal infection in augmentation of AMD phenotype, with the aid of a pioneering AMD+PD murine model established in our laboratory.

scholarly journals PEROXYNITRITE (ONOO) MEDIATES DNA DAMAGE IN CYTOKINE/LEAD TREATED MOUSE HEPATOCYTES

1997 ◽  
Vol 75 ◽  
pp. 104
Author(s):  
Ruth E. Billings ◽  
Susan M. LaRue ◽  
David J. Sieg
Keyword(s):  
Dna Damage ◽  
Treated Mouse ◽  
Mouse Hepatocytes

Reorganization of horizontal cell processes in the developing FVB/N mouse retina

2001 ◽  
Vol 306 (2) ◽  
pp. 341-346 ◽  
Author(s):  
Sung-Jin Park ◽  
In-Beom Kim ◽  
Kyu-Ryong Choi ◽  
Jung-Il Moon ◽  
Su-Ja Oh ◽  
...  
Keyword(s):  
Horizontal Cell ◽  
Mouse Retina ◽  
Cell Processes
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