Regulation of adhesion-related protein tyrosine kinases during in vitro differentiation of retinal pigment epithelial cells: translocation of pp60c-src to the nucleus is accompanied by downregulation of pp125FAK

1994 ◽  
Vol 72 (1-2) ◽  
pp. 43-48 ◽  
Author(s):  
Anna Moszczynska ◽  
Michal Opas

In the present report we show that induction of expression of a differentiated phenotype in cultured retinal pigmented epithelium of chick embryo is accompanied by coordinate regulation of expression and distribution of two adhesion-related nonreceptor protein tyrosine kinases, pp60c-src and pp125FAK∙pp60c-src translocates from the cell surface in flat undifferentiated cells to the nucleus in the packed differentiated cells. In contrast, pp125FAK, abundant in focal adhesions of flat undifferentiated cells, is downregulated in cells that have differentiated and packed into an epithelial sheet.Key words: retinal pigment epithelium, retina, tyrosine kinases, adhesion, differentiation.

Planta Medica ◽  
2008 ◽  
Vol 74 (03) ◽  
Author(s):  
Y Ye ◽  
LG Lin ◽  
H Xie ◽  
HL Li ◽  
HL Jiang ◽  
...  

2018 ◽  
Vol 25 (13) ◽  
pp. 1480-1500 ◽  
Author(s):  
Sho-ichi Yamagishi ◽  
Takanori Matsui

Pigment epithelium-derived factor (PEDF) is a glycoprotein that belongs to the superfamily of serine protease inhibitors, serpins. It was first identified as a neuronal differentiating factor secreted by human retinal pigment epithelial cells, and then found to be the most potent inhibitor of pathological angiogenesis in mammalian eyes. Recently, PEDF has been shown not only to suppress oxidative stress and inflammatory reactions in vascular wall cells, T cells and macrophages, and adipocytes, but also to exert antithrombotic and anti-fibrotic properties, thereby protecting against the development and progression of various cardiometabolic diseases and related complications. Furthermore, accumulating evidence has suggested that circulating PEDF levels may be a biomarker of severity and prognosis of these devastating disorders. Number of subjects with visceral obesity and insulin resistance is increasing, and the metabolic syndrome and its related complications, such as diabetes, nonalcoholic fatty liver disease/non-alcoholic steatohepatits, and atherosclerotic cardiovascular disease are a growing health challenge. Therefore, in this study, we review the pathophysiological role of PEDF in obesity and metabolic disorders, cardiovascular disease, diabetic eye and kidney complications, liver diseases, and reproductive system disorders, and discuss the potential clinical utility of modulating the expression and actions of PEDF for preventing these cardiometabolic disorders. We also refer to the clinical value of PEDF as a biomarker in cardiometabolic complications.


Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 179
Author(s):  
Laurence Klipfel ◽  
Marie Cordonnier ◽  
Léa Thiébault ◽  
Emmanuelle Clérin ◽  
Frédéric Blond ◽  
...  

Age-related macular degeneration (AMD) is a blinding disease for which most of the patients remain untreatable. Since the disease affects the macula at the center of the retina, a structure specific to the primate lineage, rodent models to study the pathophysiology of AMD and to develop therapies are very limited. Consequently, our understanding relies mostly on genetic studies highlighting risk alleles at many loci. We are studying the possible implication of a metabolic imbalance associated with risk alleles within the SLC16A8 gene that encodes for a retinal pigment epithelium (RPE)-specific lactate transporter MCT3 and its consequences for vision. As a first approach, we report here the deficit in transepithelial lactate transport of a rare SLC16A8 allele identified during a genome-wide association study. We produced induced pluripotent stem cells (iPSCs) from the unique patient in our cohort that carries two copies of this allele. After in vitro differentiation of the iPSCs into RPE cells and their characterization, we demonstrate that the rare allele results in the retention of intron 2 of the SLC16A8 gene leading to the absence of MCT3 protein. We show using a biochemical assay that these cells have a deficit in transepithelial lactate transport.


1998 ◽  
Vol 246 (2) ◽  
pp. 375-377 ◽  
Author(s):  
Marek Pawlikowski ◽  
Lilla Lachowicz ◽  
Jolanta Kunert-Radek ◽  
Katarzyna Winczyk ◽  
Grażyna Janiszewska ◽  
...  

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