Asymmetric dimethylarginine aggravates blood–retinal barrier breakdown of diabetic retinopathy via inhibition of intercellular communication in retinal pericytes

Amino Acids ◽  
2019 ◽  
Vol 51 (10-12) ◽  
pp. 1515-1526 ◽  
Author(s):  
Chu-Yi Huang ◽  
Ting Zhou ◽  
Ge Li ◽  
Ming-Yuan Li ◽  
Xiao-Ming Xiong ◽  
...  
2010 ◽  
Vol 176 (3) ◽  
pp. 1517-1524 ◽  
Author(s):  
Jeong-Hun Kim ◽  
Jin Hyoung Kim ◽  
Hyoung-Oh Jun ◽  
Young Suk Yu ◽  
Kyu-Won Kim

2019 ◽  
Vol 44 (10) ◽  
pp. 1133-1143 ◽  
Author(s):  
Ghulam Mohammad ◽  
Ghada Maher Abdelaziz ◽  
Mohammad Mairaj Siddiquei ◽  
Ajmal Ahmad ◽  
Gert De Hertogh ◽  
...  

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-4 ◽  
Author(s):  
Yasuo Yanagi

The retinal vessels have two barriers: the retinal pigment epithelium and the retinal vascular endothelium. Each barrier exhibits increased permeability under various pathological conditions. This condition is referred to as blood retinal barrier (BRB) breakdown. Clinically, the most frequently encountered condition causing BRB breakdown is diabetic retinopathy. In recent studies, inflammation has been linked to BRB breakdown and vascular leakage in diabetic retinopathy. Biological support for the role of inflammation in early diabetes is the adhesion of leukocytes to the retinal vasculature (leukostasis) observed in diabetic retinopathy. is a member of a ligand-activated nuclear receptor superfamily and plays a critical role in a variety of biological processes, including adipogenesis, glucose metabolism, angiogenesis, and inflammation. There is now strong experimental evidence to support the theory that inhibits diabetes-induced retinal leukostasis and leakage, playing an important role in the pathogenesis of diabetic retinopathy. Therapeutic targeting of may be beneficial to diabetic retinopathy.


2010 ◽  
Vol 51 (3) ◽  
pp. 1659 ◽  
Author(s):  
Jeong-Hun Kim ◽  
Jin Hyoung Kim ◽  
Young Suk Yu ◽  
Bon Hong Min ◽  
Kyu-Won Kim

PLoS ONE ◽  
2011 ◽  
Vol 6 (3) ◽  
pp. e17462 ◽  
Author(s):  
Laura Kowalczuk ◽  
Elodie Touchard ◽  
Samy Omri ◽  
Laurent Jonet ◽  
Christophe Klein ◽  
...  

2006 ◽  
Vol 34 (6) ◽  
pp. 584-589 ◽  
Author(s):  
Yun-Hsiang Chang ◽  
Po-Liang Chen ◽  
Ming-Cheng Tai ◽  
Chiao-Hong Chen ◽  
Da-Wen Lu ◽  
...  

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1122 ◽  
Author(s):  
Manju L. Subramanian ◽  
Thor D. Stein ◽  
Nicole Siegel ◽  
Steven Ness ◽  
Marissa G. Fiorello ◽  
...  

Animal studies have shown diabetes-induced lysyl oxidase (LOX) upregulation promotes blood-retinal-barrier breakdown and retinal vascular cell loss associated with diabetic retinopathy (DR). However, it is unclear whether changes in LOX expression contribute to the development and progression of DR. To determine if vitreous LOX levels are altered in patients with DR, 31 vitreous specimens from subjects with advanced proliferative DR (PDR), and 27 from non-diabetics were examined. The two groups were age- and gender-matched (57 ± 12 yrs vs. 53 ± 18 yrs; 19 males and 12 females vs. 17 males and 10 females). Vitreous samples obtained during vitrectomy were assessed for LOX levels using ELISA. LOX was detected in a larger number of PDR subjects (58%) than in non-diabetic subjects (15%). Additionally, ELISA measurements showed a significant increase in LOX levels in the diabetic subjects with PDR, compared to those of non-diabetic subjects (68.3 ± 112 ng/mL vs. 2.1 ± 8.2 ng/mL; p < 0.01). No gender difference in vitreous LOX levels was observed in either the diabetic or non-diabetic groups. Findings support previous reports of increased LOX levels in retinas of diabetic animals and in retinal vascular cells in high glucose condition, raising the prospect of targeting LOX overexpression as a potential target for PDR treatment.


2000 ◽  
Vol 35 (5) ◽  
pp. 233-239 ◽  
Author(s):  
Stanley A. Vinores ◽  
M.S. Seo ◽  
N. Okamoto ◽  
J.D. Ash ◽  
E.F. Wawrousek ◽  
...  

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