4.5 Article

Knockdown of Malat1 alleviates high-glucose-induced angiogenesis through regulating miR-205-5p/VEGF-A axis

Journal

EXPERIMENTAL EYE RESEARCH
Volume 207, Issue -, Pages -

Publisher

ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.exer.2021.108585

Keywords

Diabetic retinopathy; Endothelial-mesenchymal transition; Malat1; VEGF-A; miR-205-5p

Categories

Funding

  1. Joint Special Funds for the Yunnan Provincial Science and Technology Department-Kunming Medical University [2019FE001(-112)]
  2. Yunnan health training project of high level talents [H-2019023]

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This study investigated the role of Malat1 in diabetic retinopathy (DR), revealing that Malat1 regulates hRMEC dysfunction by modulating the miR-205-5p/VEGF-A pathway under high glucose conditions. The findings provide valuable insights for exploring new therapeutic targets for DR.
Diabetic retinopathy (DR), characterized by intraretinal vessel formation, is a major complication in diabetes. Neovascularization is an important characteristic of DR, but its formation mechanism remains unclear. In this research, Malat1, miR-205-5p, and VEGF-A levels in high glucose (HG) treat-human retinal microvascular endothelial cells (hRMECs) was detected with qRT-PCR. CCK-8 assay, transwell assay, and tube formation assay was applied to access hRMEC viability, migration, and angiogenesis. Expression level of endothelialmesenchymal transition (EndMT) markers (VE-cadherin, FSP1, and alpha-SMA) was detected by western blotting assay. Interaction among Malat1, miR-205-5p, and VEGF-A was confirmed by dual-luciferase reporter assay. Furthermore, in vivo DR mouse model was induced, and the effect of Malat1 on DR and EndMT markers was confirmed through hematoxylin-eosin (HE) staining and western blotting. As a result, Malat1 and VEGF-A was upregulated while miR-205-5p was suppressed under HG conditions. Malat1 could sponge miR-205-5p to regulate VEGF-A expression. Malat1 knockdown inhibited hRMEC proliferation, migration, and tube formation by targeting miR-205-5p under HG conditions. Furthermore, inhibition of Malat1 prevented the HG-induced EndMT process. In summary, Malat1 knockdown diminished hRMEC dysfunctions by regulating miR-205-5p/ VEGF-A, providing a useful insight for exploring new therapeutic target for DR.

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