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长链非编码 RNA ATP2B2-IT2 在糖尿病视网膜病变新生血管化中的初步研究。

Preliminary research on LncRNA ATP2B2-IT2 in neovascularization of diabetic retinopathy.

机构信息

Department of Ophthalmology, Zunyi First People's Hospital, The Third Affiliated Hospital of Zunyi Medical University, Zunyi, China.

Zunyi Medical University, Zunyi, China.

出版信息

BMC Ophthalmol. 2024 Jun 21;24(1):267. doi: 10.1186/s12886-024-03523-5.

DOI:10.1186/s12886-024-03523-5
PMID:38907191
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11191339/
Abstract

OBJECTIVE

Diabetic retinopathy (DR) is a common complication of diabetes, and recent findings have shown that long noncoding RNAs (lncRNAs) may be involved in its pathogenesis. Through bioinformatics analysis, we found that lncRNA ATP2B2-IT2 may be involved in this process. This study primarily investigated the expression of the lncRNA ATP2B2-IT2 in human retinal microvascular endothelial cells (HRMECs) under high-glucose conditions and its effects on HRMEC proliferation, migration, and neovascularization.

METHODS

We used RT‒PCR to assess the expression levels of lncRNA ATP2B2-IT2 and vascular endothelial growth factor (VEGF) in HRMECs under normal glucose (5.5 mmol/L) and high glucose (30 mmol/L) conditions. HRMECs were subsequently divided into four groups: the normal glucose (NG), high glucose (HG), high glucose with lncRNA ATP2B2-IT2 silencing (HG + si-lncRNA ATP2B2-IT2), and high glucose with silencing control (HG + si-NC) groups. The expression levels of the lncRNA ATP2B2-IT2 and VEGF in each group were determined using RT‒PCR. Thereafter, cell proliferation, migration, and neovascularization were assessed using CCK-8, Transwell, and tube formation assays, respectively.

RESULTS

RT‒PCR revealed that the expression levels of the lncRNA ATP2B2-IT2 and VEGF were greater in the HG group than in the NG group (P < 0.05). After silencing of the lncRNA ATP2B2-IT2, the expression of VEGF decreased significantly (P < 0.05). Subsequent CCK-8, Transwell, and tube formation assays demonstrated that compared to those in the NG group, the HRMECs in the HG group exhibited significantly increased proliferation, migration, and neovascularization (P < 0.05). However, after silencing of the lncRNA ATP2B2-IT2, the proliferation, migration, and neovascularization of HRMECs were significantly decreased in the HG + si-lncRNA ATP2B2-IT2 group compared to those in the HG group (P < 0.05).

CONCLUSION

LncRNA ATP2B2-IT2 may promote the proliferation, migration and neovascularization of HRMECs under high-glucose conditions.

摘要

目的

糖尿病视网膜病变(DR)是糖尿病的一种常见并发症,最近的研究结果表明,长链非编码 RNA(lncRNA)可能参与其发病机制。通过生物信息学分析,我们发现 lncRNA ATP2B2-IT2 可能参与了这一过程。本研究主要探讨了 lncRNA ATP2B2-IT2 在高糖环境下人视网膜微血管内皮细胞(HRMEC)中的表达及其对 HRMEC 增殖、迁移和新生血管形成的影响。

方法

采用 RT-PCR 检测正常葡萄糖(5.5mmol/L)和高葡萄糖(30mmol/L)条件下 HRMEC 中 lncRNA ATP2B2-IT2 和血管内皮生长因子(VEGF)的表达水平。随后将 HRMEC 分为正常葡萄糖组(NG)、高葡萄糖组(HG)、高葡萄糖加 lncRNA ATP2B2-IT2 沉默组(HG+si-lncRNA ATP2B2-IT2)和高葡萄糖加沉默对照组(HG+si-NC)。采用 RT-PCR 检测各组 lncRNA ATP2B2-IT2 和 VEGF 的表达水平。然后,采用 CCK-8 法、Transwell 法和管形成实验分别检测细胞增殖、迁移和新生血管形成。

结果

RT-PCR 结果显示,HG 组 lncRNA ATP2B2-IT2 和 VEGF 的表达水平均高于 NG 组(P<0.05)。沉默 lncRNA ATP2B2-IT2 后,VEGF 的表达显著降低(P<0.05)。随后的 CCK-8 法、Transwell 法和管形成实验结果表明,与 NG 组相比,HG 组 HRMEC 的增殖、迁移和新生血管形成能力均显著增强(P<0.05)。然而,沉默 lncRNA ATP2B2-IT2 后,HG+si-lncRNA ATP2B2-IT2 组 HRMEC 的增殖、迁移和新生血管形成能力较 HG 组显著降低(P<0.05)。

结论

在高糖条件下,lncRNA ATP2B2-IT2 可能促进 HRMEC 的增殖、迁移和新生血管形成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d569/11191339/ff0965bf6fdf/12886_2024_3523_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d569/11191339/8c1eb0c44362/12886_2024_3523_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d569/11191339/16b049542a49/12886_2024_3523_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d569/11191339/675e725cdcf1/12886_2024_3523_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d569/11191339/95f3ceb2d43a/12886_2024_3523_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d569/11191339/ff0965bf6fdf/12886_2024_3523_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d569/11191339/8c1eb0c44362/12886_2024_3523_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d569/11191339/16b049542a49/12886_2024_3523_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d569/11191339/38a54160cbf7/12886_2024_3523_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d569/11191339/675e725cdcf1/12886_2024_3523_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d569/11191339/95f3ceb2d43a/12886_2024_3523_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d569/11191339/ff0965bf6fdf/12886_2024_3523_Fig6_HTML.jpg

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