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自噬相关蛋白16样蛋白1(ATG16L1)促进高糖诱导的视网膜毛细血管内皮细胞的迁移和侵袭。

ATG16L1 promotes cell migration and invasion in high glucose-induced retinal capillary endothelial cells.

作者信息

Gao Xinxiao, Xie Pinxue, Feng Wen, Han Jindong, Tan Xiaobo

机构信息

Department of Ophthalmology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.

Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.

出版信息

Front Med (Lausanne). 2025 Jul 15;12:1515936. doi: 10.3389/fmed.2025.1515936. eCollection 2025.

DOI:10.3389/fmed.2025.1515936
PMID:40735446
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12303877/
Abstract

PURPOSE

Diabetic retinopathy (DR), a common chronic complication of diabetes, often results in irreversible visual dysfunction. This study investigated the mechanisms underlying the expression of ATG16L1, a potential biomarker of DR.

METHODS

We investigated the role of ATG16L1 in high glucose (HG)-induced retinal capillary endothelial cells (RCECs). Rat RCECs were cultured in normal glucose (NG) or HG medium with or without ATG16L1 transfection.

RESULTS

The mRNA and protein expression levels of ATG16L1 were significantly upregulated in RCECs exposed to HG medium. The migration ability and invasion rate of RCECs were significantly higher in the HG group than in the NG group but decreased markedly after transfection with ATG16L1 siRNA, compared with those in the control group ( < 0.01).

CONCLUSION

ATG16L1 might be involved in the development of DR by promoting the migration of RCECs.

摘要

目的

糖尿病视网膜病变(DR)是糖尿病常见的慢性并发症,常导致不可逆的视觉功能障碍。本研究探讨了自噬相关基因16样蛋白1(ATG16L1)作为DR潜在生物标志物表达的潜在机制。

方法

我们研究了ATG16L1在高糖(HG)诱导的视网膜毛细血管内皮细胞(RCECs)中的作用。将大鼠RCECs培养在正常葡萄糖(NG)或HG培养基中,转染或未转染ATG16L1。

结果

暴露于HG培养基的RCECs中,ATG16L1的mRNA和蛋白表达水平显著上调。HG组RCECs的迁移能力和侵袭率显著高于NG组,但与对照组相比,转染ATG16L1小干扰RNA后显著降低(<0.01)。

结论

ATG16L1可能通过促进RCECs的迁移参与DR的发生发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a999/12303877/26450a279d00/fmed-12-1515936-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a999/12303877/5dfa159ee1f9/fmed-12-1515936-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a999/12303877/35c364675067/fmed-12-1515936-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a999/12303877/a99ff17770af/fmed-12-1515936-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a999/12303877/26450a279d00/fmed-12-1515936-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a999/12303877/5dfa159ee1f9/fmed-12-1515936-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a999/12303877/35c364675067/fmed-12-1515936-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a999/12303877/a99ff17770af/fmed-12-1515936-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a999/12303877/26450a279d00/fmed-12-1515936-g004.jpg

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