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参与抗血管内皮生长因子诱导的视网膜色素上皮细胞上皮间质转化

Participates in Anti-VEGF-Induced Epithelial Mesenchymal Transformation in RPE Cells.

作者信息

Hao Xianghui, Hua Yingbin, Xie Chaohui, Xu Haifeng

机构信息

State Key Laboratory Cultivation Base, Shandong Provincial Key Laboratory of Ophthalmology, Shandong Eye Institute, Shandong First Medical University & Shandong Academy of Medical Sciences, Qingdao, People's Republic of China.

Qingdao Eye Hospital, Shandong First Medical University & Shandong Academy of Medical Sciences, Qingdao, People's Republic of China.

出版信息

Clin Ophthalmol. 2023 Oct 16;17:3047-3056. doi: 10.2147/OPTH.S427894. eCollection 2023.

DOI:10.2147/OPTH.S427894
PMID:37869043
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10588660/
Abstract

BACKGROUND

To explore the role and possible mechanism of in anti-VEGF drug-induced epithelial-mesenchymal transformation (EMT) in human retinal pigment epithelium (ARPE-19) cells, and to seek more therapeutic targets to improve prognosis vision.

METHODS

ARPE-19 cells were exposed to clinical dosage of bevacizumab and expression was measured by real-time polymerase chain reaction (RT-PCR) assay. mimic and inhibitor were transfected into bevacizumab-induced ARPE-19, the expression of , and were detected by cell immunofluorescence and Western blotting.

RESULTS

Clinical dosage of bevacizumab caused EMT and enhanced expression in ARPE-19 cells (P<0.05). The inhibition of attenuated the EMT effect of bevacizumab, while overexpression of promoted this activity (P<0.05). The SNAI1 was up-regulated by bevacizumab and promotion was partially suppressed by the inhibitor and aggravated by the mimic (P<0.05).

CONCLUSION

promotes bevacizumab-induced EMT in ARPE cells which is significantly positively correlated with might be a potential miRNA-based therapeutic target for reducing bevacizumab-induced subretinal fibrosis.

摘要

背景

探讨[具体内容缺失]在抗血管内皮生长因子（VEGF）药物诱导的人视网膜色素上皮（ARPE - 19）细胞上皮 - 间质转化（EMT）中的作用及可能机制，寻找更多改善预后视力的治疗靶点。

方法

将ARPE - 19细胞暴露于临床剂量的贝伐单抗，并通过实时聚合酶链反应（RT - PCR）检测[具体内容缺失]的表达。将[具体内容缺失]模拟物和抑制剂转染到贝伐单抗诱导的ARPE - 19细胞中，通过细胞免疫荧光和蛋白质印迹法检测[具体内容缺失]、[具体内容缺失]和[具体内容缺失]的表达。

结果

临床剂量的贝伐单抗导致ARPE - 19细胞发生EMT并增强[具体内容缺失]的表达（P < 0.05）。抑制[具体内容缺失]减弱了贝伐单抗的EMT作用，而过表达[具体内容缺失]则促进了这种作用（P < 0.05）。贝伐单抗上调了SNAI1，[具体内容缺失]抑制剂部分抑制了其上调作用，而[具体内容缺失]模拟物则加剧了这种上调作用（P < 0.05）。

结论

[具体内容缺失]促进贝伐单抗诱导的ARPE细胞EMT，这与[具体内容缺失]显著正相关，[具体内容缺失]可能是减少贝伐单抗诱导的视网膜下纤维化的潜在基于微小RNA的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738c/10588660/029f4bf0eb4f/OPTH-17-3047-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738c/10588660/a8760e085fd7/OPTH-17-3047-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738c/10588660/9fcf94260289/OPTH-17-3047-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738c/10588660/08c3d86a44dc/OPTH-17-3047-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738c/10588660/7bb91b089210/OPTH-17-3047-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738c/10588660/78b1b09c38c8/OPTH-17-3047-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738c/10588660/b0fa904b4489/OPTH-17-3047-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738c/10588660/08d19deed47c/OPTH-17-3047-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738c/10588660/029f4bf0eb4f/OPTH-17-3047-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738c/10588660/a8760e085fd7/OPTH-17-3047-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738c/10588660/9fcf94260289/OPTH-17-3047-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738c/10588660/08c3d86a44dc/OPTH-17-3047-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738c/10588660/7bb91b089210/OPTH-17-3047-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738c/10588660/78b1b09c38c8/OPTH-17-3047-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738c/10588660/b0fa904b4489/OPTH-17-3047-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738c/10588660/08d19deed47c/OPTH-17-3047-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738c/10588660/029f4bf0eb4f/OPTH-17-3047-g0008.jpg

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