<i>VEGF</i>-mediated angiogenesis in retinopathy of prematurity is co-regulated by miR-17-5p and miR-20a-5p

Guo, Yan; Du, Fei; Tan, Yilan; Luo, Jun; Xiong, Dan; Song, Wook

doi:10.1139/bcb-2020-0357

Cited by 12 publications

(10 citation statements)

References 28 publications

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“…Some of them played the same role in both processes. For example, high level of VEGF resulted in retinal vasculature, while reducing VEGF induced by hyperoxia treatment in OIR model led to neovascular tufts [32] . Erythropoietin (EPO) deficiency decreased retinal vascular stability, and intravitreal injection of EPO siRNA effectively suppressed retinal neovascularization [33][34] .…”

Section: Discussionmentioning

confidence: 99%

Procollagen C-proteinase enhancer 1 promotes physiologic retinal angiogenesis via regulating the process of collagen

Luo¹,

Chen²,

Liu³

et al. 2022

Int J Ophthalmol

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AIM: To investigate the role of procollagen C-proteinase enhancer 1 (PCPE1) in retinal angiogenesis and relevant mechanisms. METHODS: The Pcolce1-knockout (KO) mice were used to explore the effect of PCPE1 on retinal angiogenesis in vivo. Pcolce1 siRNA were designed, cell count kit 8 (CCK8) assays and tube formation assays were performed to investigate the cell proliferation and tube formation abilities of retinal microvascular endothelial cells (hRMECs) in vitro. Mouse embryo fibroblasts (MEF) cells were isolated and cultured to analyze the effect of PCPE1 on enhancing procollagen cleavage. RESULTS: In vivo studies showed that the retinal vascular density of Pcolce1-/- mice was significantly lower than that of the control group. Furthermore, silencing of Pcolce1 inhibited cell proliferation and tube formation abilities of hRMECs in vitro. Additionally, much more pro-collagen was found in Pcolce1-/- MEF cells, compared to wild type MEF cells. CONCLUSION: PCPE1 may promote physiological retinal angiogenesis by regulating the processing of collagen, which may provide a potential therapeutic target of retinal vascular disease.

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Section: Discussionmentioning

confidence: 99%

Procollagen C-proteinase enhancer 1 promotes physiologic retinal angiogenesis via regulating the process of collagen

Luo¹,

Chen²,

Liu³

et al. 2022

Int J Ophthalmol

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“…The OIR model is commonly used to study retinal vascular diseases, including ROP because it simulates the relative hypoxia stage of ROP created by hyperoxia followed by normoxia ( 26 , 27 ). Many previous reports have described miR-145-5p as a target gene of TUG1 , and that knockdown of TUG1 can inhibit cell migration and damage, which may have a protective effect on cells via targeting miR-145-5p ( 28 – 30 ).…”

Section: Discussionmentioning

confidence: 99%

LncRNA TUG1 Promotes Apoptosis, Invasion, and Angiogenesis of Retinal Endothelial Cells in Retinopathy of Prematurity via MiR-145-5p

Wang

et al. 2022

Front. Med.

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PurposeRetinopathy of prematurity (ROP) is a common retinal vascular disease in premature neonates. In recent years, there is increasing evidence that the long non-coding RNA taurine upregulated gene 1 (TUG1) plays a regulatory role in vascular diseases, suggesting a potential role for TUG1 in vascular endothelial cells. We hypothesized that TUG1 may be associated with ROP. Our aim, therefore, was to explore the biological functions of TUG1 in aberrant retinal development.MethodsWe used the mouse oxygen-induced retinopathy (OIR) model to simulate the pathological changes of retinal in ROP. Quantitative real-time polymerase chain reaction was used to detect the expression of TUG1, miR-145-5p and cellular communication network factor 1 (CCN1). Human retinal endothelial cells (HRECs) were treated with CoCl2 to mimic hypoxia conditions. Cellular functional changes were observed after transfection with RNA interference (RNAi)-TUG1 and miR-145-5p mimics. The apoptosis of HRECs was detected by flow cytometry, the migration ability was detected by wound healing and transwell migration assays, and the ability of angiogenesis was detected by tube formation assay. The potential binding sites between TUG1, miR-145-5p, and CCN1 were verified by dual-luciferase reporter assays. The degree of retinopathy was evaluated by staining retinal sections with hematoxylin and eosin, and the expression of CCN1, HIF-1α, VEGF, caspase-3, Bcl-2, IL-1β, and TNF-α protein was analyzed by Western blotting and immunohistochemistry.ResultsIn the retina tissue of OIR mice, TUG1, miR-145-5p, and CCN1 were differentially expressed. Knocking down TUG1 attenuated apoptosis, migration, and angiogenesis induced by hypoxia on HRECs, as did miR-145-5p overexpression. Results from reporter assays indicate direct interactions between TUG1, miR-145-5p, and CCN1. Intravitreal injection of miR-145-5p mimics reduced the degree of retinopathy.ConclusionTUG1 acts as a molecular sponge of miR-145-5p to regulate CCN1 expression and thus regulate the development of retinal neovascularization. This regulatory mechanism may provide a new theoretical basis for the prevention and treatment of ROP.

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“…On this basis, we predicted that miR-106a-5p may be involved in the regulation of MMP-2 expression through MALAT1. In in vivo experiments, an OIR model was employed that simulates the relative hypoxic phases of ROP induced by hyperoxia and normoxia [25,26] . The experimental results showed that the OIR model had a signi cant decrease in the expression of miR-106a-5p and an increase in the expression of MALAT1 and MMP-2; in addition, overexpression of miR-106a-5p could reverse these effects.…”

Section: Discussionmentioning

confidence: 99%

Long-chain non-coding RNA MALAT1 upregulates the MMP-2 signaling pathway by inhibiting miR-106a-5p in murine oxygen- induced retinopathy

et al. 2022

Preprint

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Retinopathy of prematurity (ROP) is a blinding eye disease in children that is characterized by the formation of neovascularization in the retina; current treatments for this disease risk retinal damage and visual impairment. This study aimed to investigate the relationship between metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), miR-106a-5p, and matrix metalloproteinase 2 (MMP-2) in an oxygen-induced retinopathy mouse model and hypoxia-induced human retinal endothelial cells and to elucidate whether MALAT1 upregulates MMP-2 signaling by inhibiting miR-106a-5p. The role of this pathway in oxygen-induced murine retinopathy and its underlying mechanism were also investigated. MALAT1 inhibited the expression of miR-106a-5p and enhanced the expression of MMP-2, which in turn caused a series of pathological changes, such as the formation of new blood vessels in the retina. In addition, knockdown of MALAT1 can downregulate the expression of MMP-2 by sponging miR-106a-5p and inhibiting cell proliferation, migration, and tube-forming ability. In conclusion, our findings suggest that MALAT1 may contribute to the occurrence and development of ROP by inhibiting miR-106a-5p and increasing the expression of MMP-2, thus providing a new perspective for the targeted therapy of ROP.

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VEGF-mediated angiogenesis in retinopathy of prematurity is co-regulated by miR-17-5p and miR-20a-5p

Cited by 12 publications

References 28 publications

Procollagen C-proteinase enhancer 1 promotes physiologic retinal angiogenesis via regulating the process of collagen

Procollagen C-proteinase enhancer 1 promotes physiologic retinal angiogenesis via regulating the process of collagen

LncRNA TUG1 Promotes Apoptosis, Invasion, and Angiogenesis of Retinal Endothelial Cells in Retinopathy of Prematurity via MiR-145-5p

Long-chain non-coding RNA MALAT1 upregulates the MMP-2 signaling pathway by inhibiting miR-106a-5p in murine oxygen- induced retinopathy

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