Advanced glycation end (AGE) product modification of laminin downregulates Kir4.1 in retinal Müller cells

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Advanced glycation end (AGE) product modification of laminin downregulates Kir4.1 in retinal Müller cells

Diabetic retinopathy (DR) is a major cause of adult blindness. Retinal Müller cells maintain water homeostasis and potassium concentration via inwardly rectifying Kir4.1 channels. Accumulation of advanced glycation end products (AGEs) is a major pathologic event in DR. While diabetes leads to a decrease in the Kir4.1 channels, it remains unknown whether AGEs-linked to the basement membrane (BM)...

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Advanced glycation end-products stimulate basic fibroblast growth factor expression in cultured Müller cells

Accumulating evidence points to a causal role for advanced glycation end-products (AGEs) in the development of diabetic vascular complications, including diabetic retinopathy (DR). To assess the reciprocal correlation between AGEs and basic fibroblast growth factor (bFGF), the effects of AGEs on the production of bFGF by Müller cells were investigated. Müller cells were cultured from adult rabb...

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ژورنال

عنوان ژورنال: PLOS ONE

سال: 2018

ISSN: 1932-6203

DOI: 10.1371/journal.pone.0193280