Amyloid-beta mediates the receptor of advanced glycation end product-induced pro-inflammatory response via toll-like receptor 4 signaling pathway in retinal ganglion cell line RGC-5

The International Journal of Biochemistry & Cell Biology
Jong-Jer LeeJiin-Haur Chuang

Abstract

Patients with diabetes mellitus have an increased risk of developing Alzheimer's disease. Amyloid-β, a product of amyloid precursor protein, is associated with neuro-inflammation in patients with Alzheimer's diseases. The correlation between amyloid-beta and advanced glycation end products, which accumulate in tissue of diabetic patients, is not clear. The aims of this study were to determine the effect of advanced glycation end product on the expression of amyloid precursor protein/amyloid-beta and associated pro-inflammatory responses in retinal ganglion cell line RGC-5. Treatment with advanced glycation end product produced upregulation of amyloid precursor protein and increased secretion of amyloid-β(1-40). Additionally, amyloid-β(1-40) induced toll-like receptor 4-dependent phosphorylation of tyrosine in myeloid differentiation primary response gene (88). We found that N-[N-(3,5-Difluorophenacetyl)-l-alanyl]-S-phenylglycine t-butyl ester, a γ-secretase inhibitor, reduced the secretion of amyloid-β(1-40) and inhibited the advanced glycation end product-induced activation of myeloid differentiation primary response gene (88). Amyloid-β(1-40) induced the activation of NF-κB and the expression of TNFα mRNA. Knockdown of toll-l...Continue Reading

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Citations

Mar 11, 2016·American Journal of Reproductive Immunology : AJRI·Koumei ShirasunaTakehito Kuwayama
Jul 11, 2020·Medicinal Research Reviews·Xu WangGuang Liang
Apr 24, 2020·Laboratory Investigation; a Journal of Technical Methods and Pathology·Yasunari Munemasa
Dec 10, 2020·Inflammation and Regeneration·Kento Otani, Takashi Shichita

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