Development of Proliferative Vitreoretinopathy Is Attenuated by Chicken Ovalbumin Upstream Promoter Transcriptional Factor 1 Via Inhibiting Epithelial-Mesenchymal Transition.

IF 2.1 4区 医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
Discovery medicine Pub Date : 2022-09-01
Huizi Jin, Wenting Cai, Donghui Yu, Jiaqi Fan, Qingyu Liu, Jing Yu
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引用次数: 0

Abstract

Proliferative vitreoretinopathy (PVR) is an intractable condition after rhegmatogenous retinal detachment (RD), which is the primary cause of failure in retinal reattachment surgery. This study aimed to investigate the effects of chicken ovalbumin upstream promoter transcriptional factor 1 (COUP-TF1) in the development of proliferative vitreoretinopathy (PVR) both in vitro and in vivo. Adult retinal pigment epithelium cell line was used for in-vitro experiments. Immunocytochemistry assay, real-time quantitative polymerase chain reaction, and Western blot were used to measure the expression of COUP-TF1, alpha-smooth muscle actin (α-SMA), and E-cadherin. Epithelial-mesenchymal transition (EMT) was observed through cell counting kit-8 assay, wound healing tests, and the expression changes of related proteins. PVR rabbit models were established and evaluated by the images of fundus and vitreous cavity, pathological sections, and COUP-TF1 expression. As shown by our results, the proliferation and migration of the COUP-TF1 knockdown cells were reduced compared with the control cells with or without transforming growth factor-β1 (TGF-β1) treatment. After TGF-β1 treatment, α-SMA expression was upregulated in ARPE-19 cells but kept the same in COUP-TF1 knockdown cells. E-cadherin expression was down-regulated in all the groups but the extent of the decrease in COUP-TF1 knockdown cells was smaller. EMT was attenuated in ARPE-19 cells after COUP-TF1 was knocked down. In the in-vivo experiment, PVR severity was attenuated and the retinal detachment rate decreased on the 14th and 28th day in COUP-TF1 knockdown group. In conclusion, COUP-TF1 is related to the development of PVR, and COUP-TF1 knockdown attenuates the progression of PVR. This suggests that COUP-TF1 can be a promising candidate for the treatment of PVR.

鸡卵白蛋白上游启动子转录因子1通过抑制上皮-间质转化而减弱增殖性玻璃体视网膜病变的发展。
增殖性玻璃体视网膜病变(PVR)是孔源性视网膜脱离(RD)后的顽固性疾病,是视网膜再植手术失败的主要原因。本研究旨在探讨鸡卵白蛋白上游启动子转录因子1 (COUP-TF1)在增殖性玻璃体视网膜病变(PVR)发生中的作用。体外实验采用成人视网膜色素上皮细胞系。采用免疫细胞化学法、实时定量聚合酶链反应法、Western blot法检测cbp - tf1、α-平滑肌肌动蛋白(α-SMA)、E-cadherin的表达。通过细胞计数试剂盒-8、创面愈合试验及相关蛋白表达变化观察上皮-间质转化(EMT)。建立兔PVR模型,并通过眼底、玻璃体、病理切片及COUP-TF1表达进行评价。我们的研究结果表明,与未处理转化生长因子-β1 (TGF-β1)的对照细胞相比,COUP-TF1敲低细胞的增殖和迁移能力均有所降低。TGF-β1处理后,α-SMA在ARPE-19细胞中表达上调,而在COUP-TF1敲除细胞中表达不变。E-cadherin表达在各组均下调,但COUP-TF1敲低细胞的下调幅度较小。敲除COUP-TF1后,ARPE-19细胞的EMT减弱。在体内实验中,COUP-TF1敲除组在第14天和第28天PVR严重程度减轻,视网膜脱离率降低。综上所述,COUP-TF1与PVR的发展有关,而COUP-TF1基因敲低可减缓PVR的进展。这表明COUP-TF1可能是治疗PVR的有希望的候选药物。
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来源期刊
Discovery medicine
Discovery medicine MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
5.40
自引率
0.00%
发文量
80
审稿时长
6-12 weeks
期刊介绍: Discovery Medicine publishes novel, provocative ideas and research findings that challenge conventional notions about disease mechanisms, diagnosis, treatment, or any of the life sciences subjects. It publishes cutting-edge, reliable, and authoritative information in all branches of life sciences but primarily in the following areas: Novel therapies and diagnostics (approved or experimental); innovative ideas, research technologies, and translational research that will give rise to the next generation of new drugs and therapies; breakthrough understanding of mechanism of disease, biology, and physiology; and commercialization of biomedical discoveries pertaining to the development of new drugs, therapies, medical devices, and research technology.
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