scholarly journals Critical Role of TrkB and Brain-Derived Neurotrophic Factor in the Differentiation and Survival of Retinal Pigment Epithelium

1997 ◽  
Vol 17 (22) ◽  
pp. 8749-8755 ◽  
Author(s):  
Zheng Z. Liu ◽  
Ling Q. Zhu ◽  
Fernette F. Eide
PLoS ONE ◽  
2011 ◽  
Vol 6 (9) ◽  
pp. e23148 ◽  
Author(s):  
Rong Li ◽  
Rong Wen ◽  
Tina Banzon ◽  
Arvydas Maminishkis ◽  
Sheldon S. Miller

2011 ◽  
Vol 52 (13) ◽  
pp. 9478 ◽  
Author(s):  
Knatokie M. Ford ◽  
Magali Saint-Geniez ◽  
Tony Walshe ◽  
Alisar Zahr ◽  
Patricia A. D'Amore

2020 ◽  
Vol 21 (11) ◽  
pp. 3830 ◽  
Author(s):  
Yan Levitsky ◽  
Sandra S. Hammer ◽  
Kiera P. Fisher ◽  
Chao Huang ◽  
Travan L. Gentles ◽  
...  

Mitochondrial damage in the cells comprising inner (retinal endothelial cells) and outer (retinal pigment epithelium (RPE)) blood–retinal barriers (BRB) is known to precede the initial BRB breakdown and further histopathological abnormalities in diabetic retinopathy (DR). We previously demonstrated that activation of acid sphingomyelinase (ASM) is an important early event in the pathogenesis of DR, and recent studies have demonstrated that there is an intricate connection between ceramide and mitochondrial function. This study aimed to determine the role of ASM-dependent mitochondrial ceramide accumulation in diabetes-induced RPE cell damage. Mitochondria isolated from streptozotocin (STZ)-induced diabetic rat retinas (7 weeks duration) showed a 1.64 ± 0.29-fold increase in the ceramide-to-sphingomyelin ratio compared to controls. Conversely, the ceramide-to-sphingomyelin ratio was decreased in the mitochondria isolated from ASM-knockout mouse retinas compared to wild-type littermates, confirming the role of ASM in mitochondrial ceramide production. Cellular ceramide was elevated 2.67 ± 1.07-fold in RPE cells derived from diabetic donors compared to control donors, and these changes correlated with increased gene expression of IL-1β, IL-6, and ASM. Treatment of RPE cells derived from control donors with high glucose resulted in elevated ASM, vascular endothelial growth factor (VEGF), and intercellular adhesion molecule 1 (ICAM-1) mRNA. RPE from diabetic donors showed fragmented mitochondria and a 2.68 ± 0.66-fold decreased respiratory control ratio (RCR). Treatment of immortalized cell in vision research (ARPE-19) cells with high glucose resulted in a 25% ± 1.6% decrease in citrate synthase activity at 72 h. Inhibition of ASM with desipramine (15 μM, 1 h daily) abolished the decreases in metabolic functional parameters. Our results are consistent with diabetes-induced increase in mitochondrial ceramide through an ASM-dependent pathway leading to impaired mitochondrial function in the RPE cells of the retina.


2018 ◽  
Vol 22 (11) ◽  
pp. 5244-5256 ◽  
Author(s):  
Sandra Atienzar-Aroca ◽  
Gemma Serrano-Heras ◽  
Aida Freire Valls ◽  
Carmen Ruiz de Almodovar ◽  
Maria Muriach ◽  
...  

2005 ◽  
Vol 22 (3) ◽  
pp. 251-261 ◽  
Author(s):  
JODI RYMER ◽  
CHRISTINE F. WILDSOET

Myopia is increasing in prevalence world-wide, nearing epidemic proportions in some populations. This has led to expanded research efforts to understand how ocular growth and refractive errors are regulated. Eye growth is sensitive to visual experience, and is altered by both form deprivation and optical defocus. In these cases, the primary targets of growth regulation are the choroidal and scleral layers of the eye that demarcate the boundary of the posterior vitreous chamber. Of significance to this review are observations of local growth modulation that imply that the neural retina itself must be the source of growth-regulating signals. Thus the retinal pigment epithelium (RPE), interposed between the retina and the choroid, is likely to play a critical role in relaying retinal growth signals to the choroid and sclera. This review describes the ion transporters and signal receptors found in the chick RPE and their possible roles in visually driven changes in eye growth. We focus on the effects of four signaling molecules, otherwise implicated in eye growth changes (dopamine, acetylcholine, vasoactive intestinal peptide (VIP), and glucagon), on RPE physiology, including fluid transport. A model for RPE-mediated growth regulation is proposed.


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