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晚期糖基化终产物刺激培养的 Müller 细胞中碱性成纤维细胞生长因子的表达。

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

机构信息

Department of Ophthalmology, Second Affiliated Hospital (Binjiang Branch), School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310009, PR China.

出版信息

Mol Med Rep. 2013 Jan;7(1):16-20. doi: 10.3892/mmr.2012.1152. Epub 2012 Oct 24.

DOI:10.3892/mmr.2012.1152
PMID:23129015
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3572729/
Abstract

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 rabbit retinas. The AGEs were prepared with highly glycated bovine serum albumin (BSA) and the control non‑glycated BSA (BSA control) was incubated under the same conditions without glucose. Cultured Müller cells were exposed to AGEs or BSA control (volume percentages were 4, 8, 16, 32 and 64%) for a time course of 1, 3, 6 and 9 days in their desired medium. The expression of bFGF in Müller cells was evaluated by immunocytochemistry. Quantification was performed by densitometry using computerized image analysis with dedicated software. AGEs in a volume percentage of 16 and 32% on day 1 and in a volume percentage of 16, 32 and 64% on days 3, 6 and 9 increased the bFGF expression in Müller cells (P<0.05). Additionally, AGEs upregulated bFGF expression in Müller cells in a time‑dependent manner. In conclusion, the treatment of Müller cells with AGEs resulted in a dose- and time‑dependent elevation of bFGF in the culture medium. The results from this study suggest that the increased formation of AGEs in the vitreous may be involved in the development of DR by inducing the production of bFGF by retinal Müller cells.

摘要

越来越多的证据表明,糖基化终产物(AGEs)在糖尿病血管并发症的发展中起因果作用,包括糖尿病性视网膜病变(DR)。为了评估 AGEs 与碱性成纤维细胞生长因子(bFGF)之间的相互关系,研究了 AGEs 对 Müller 细胞产生 bFGF 的影响。Müller 细胞从成年兔视网膜中培养。AGEs 是用高度糖化的牛血清白蛋白(BSA)制备的,对照非糖化 BSA(BSA 对照)在没有葡萄糖的相同条件下孵育。培养的 Müller 细胞在其所需的培养基中暴露于 AGEs 或 BSA 对照(体积百分比为 4、8、16、32 和 64%),时间为 1、3、6 和 9 天。通过免疫细胞化学评估 Müller 细胞中 bFGF 的表达。使用专用软件通过计算机化图像分析进行密度计法进行定量。第 1 天体积百分比为 16 和 32%的 AGEs 和第 3、6 和 9 天体积百分比为 16、32 和 64%的 AGEs 增加了 Müller 细胞中的 bFGF 表达(P<0.05)。此外,AGEs 以时间依赖性方式上调 Müller 细胞中的 bFGF 表达。总之,用 AGEs 处理 Müller 细胞导致培养基中 bFGF 的剂量和时间依赖性升高。本研究结果表明,玻璃体中 AGEs 的形成增加可能通过诱导视网膜 Müller 细胞产生 bFGF 而参与 DR 的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35da/3572729/0cf33f0da78b/MMR-07-01-0016-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35da/3572729/4ccee8bbd111/MMR-07-01-0016-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35da/3572729/b5e0b980b4cc/MMR-07-01-0016-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35da/3572729/bec0a0dd40e8/MMR-07-01-0016-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35da/3572729/3c4854f1e5e3/MMR-07-01-0016-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35da/3572729/0cf33f0da78b/MMR-07-01-0016-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35da/3572729/4ccee8bbd111/MMR-07-01-0016-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35da/3572729/b5e0b980b4cc/MMR-07-01-0016-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35da/3572729/bec0a0dd40e8/MMR-07-01-0016-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35da/3572729/3c4854f1e5e3/MMR-07-01-0016-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35da/3572729/0cf33f0da78b/MMR-07-01-0016-g04.jpg

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