miR-200-3p suppresses cell proliferation and reduces apoptosis in diabetic retinopathy via blocking the TGF-β2/Smad pathway

Xue, Leigang; Li, Juanjuan; Ren, Yuling; Zhang, Liwei; Jiao, Kai; Chen, Chen; Ding, Peng

doi:10.1042/bsr20201545

Cited by 18 publications

(16 citation statements)

References 38 publications

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“…These results suggested that overproliferation of RECs and retinal angiogenesis was mainly driven by high glucose rather than high osmotic pressure (26). Meanwhile, high glucose remarkably induced an increase in expressions of TGF-β1 and VEGF, and decreased expression of miR-200b in RECs, which was similar to the results in previous studies (27). However, after miR-200b mimic was transfected into RECs under high glucose condition, TGF-β1 level was also signi cantly elevated.…”

Section: Discussionsupporting

confidence: 88%

Hyperoside improves diabetic retinopathy by regulating TGF-β1/miR-200b/VEGF pathway

Zhou

et al. 2023

Preprint

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Aims To evaluate the efficacy of hyperoside and the role of TGF-β1/miR-200b/VEGF pathway in treating diabetic retinopathy (DR). Methods (1) Retinal endothelial cells (RECs) were cultured in the normal-glucose group (NG), high-glucose group (HG), mannitol group, high glucose + low-concentration hyperoside group, high glucose + high-concentration hyperoside group, normal glucose + miR-200b inhibitor group (NG + MI), normal glucose + normal control group (NG + NC), high glucose + miR-200b mimic group (HG + MM), and high glucose + normal control group (HG + NC). The viability, migration and tube formation of RECs, and the expressions of TGF-β1, miR-200b and VEGF in each group were detected and compared. (2) Eight Sprague Dawley (SD) rats were used in the normal control group, and 32 SD rats established DR models were randomly divided into the four groups for DR group (DR), DR + low-dose hyperoside group, DR + high-dose hyperoside group, and DR + Calcium Dobesilate group. The tissue pathology and vasculopathy of rat retina, and the expressions of TGF-β1, miR-200b, and VEGF of retinal tissues in different group were tested and compared. Results (1) Excessive proliferation, migration and tube formation of RECs were induced by high glucose. The expressions of TGF-β1 and VEGF in HG were markedly up-regulated, but miR-200b levels were obviously down-regulated. However, hyperoside could significantly reverse the expressions of TGF-β1, VEGF and miR-200b; and inhibit high-glucose-induced over-proliferation of RECs dose-dependently. RECs viability and VEGF level were much higher in NG + MI than for NG but lower in HG + MM than for HG, while miR-200b level was substantially lower in NG + MI than for NG but higher in HG + MM than for HG. (2) The retinal pathological changes and vasculopathy in DR rats were more serious compared with normal rats. TGF-β1 and VEGF levels in DR rats retina were markedly up-regulated, while miR-200b levels were obviously down-regulated. However, hyperoside could notably reverse the expressions of TGF-β1, VEGF, and miR-200b in DR rat retina and alleviate retinal tissue injury and vascular lesions of DR rats dose-dependently. Conclusion Hyperoside could treat DR by regulating TGF-β1/miR-200b/VEGF pathway.

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Section: Discussionsupporting

confidence: 88%

Hyperoside improves diabetic retinopathy by regulating TGF-β1/miR-200b/VEGF pathway

Zhou

et al. 2023

Preprint

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“…In the eye, many miRNAs have been found to be abundantly expressed and play important roles in ocular physiology and pathology. These include miR-200 [ 64 ] miR-184 [ 65 ] miR-29 family [ 66 ] and miR-21 [ 67 ]. Expression profiling of miRNAs in the anterior segment of healthy donors including cornea, TM, and ciliary body samples reported 378 miRs collectively expressed [ 68 ].…”

Section: Micrornas That Regulate Tgf-β Signallingmentioning

confidence: 99%

The Role of miR-29 Family in TGF-β Driven Fibrosis in Glaucomatous Optic Neuropathy

Smyth

Callaghan

Willoughby

et al. 2022

IJMS

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Primary open angle glaucoma (POAG), a chronic optic neuropathy, remains the leading cause of irreversible blindness worldwide. It is driven in part by the pro-fibrotic cytokine transforming growth factor beta (TGF-β) and leads to extracellular matrix remodelling at the lamina cribrosa of the optic nerve head. Despite an array of medical and surgical treatments targeting the only known modifiable risk factor, raised intraocular pressure, many patients still progress and develop significant visual field loss and eventual blindness. The search for alternative treatment strategies targeting the underlying fibrotic transformation in the optic nerve head and trabecular meshwork in glaucoma is ongoing. MicroRNAs are small non-coding RNAs known to regulate post-transcriptional gene expression. Extensive research has been undertaken to uncover the complex role of miRNAs in gene expression and miRNA dysregulation in fibrotic disease. MiR-29 is a family of miRNAs which are strongly anti-fibrotic in their effects on the TGF-β signalling pathway and the regulation of extracellular matrix production and deposition. In this review, we discuss the anti-fibrotic effects of miR-29 and the role of miR-29 in ocular pathology and in the development of glaucomatous optic neuropathy. A better understanding of the role of miR-29 in POAG may aid in developing diagnostic and therapeutic strategies in glaucoma.

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“…These cells were initially transfected for 6 h and then the medium was replaced with DMEM/ f-12 medium containing 30 mM high glucose (HG). After 24-h incubation, the cells were subjected to the following experiments [ 23 ].…”

Section: Methodsmentioning

confidence: 99%

Danhong injection represses diabetic retinopathy and nephropathy advancement in diabetic mice by upregulating microRNA-30d-5p and targeting JAK1

et al. 2022

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Danhong injection (DHI) restrains diabetic retinopathy and nephropathy (DR and DN) advancement in diabetic mice. However, the downstream mechanism of its modulation is not fully studied. Diabetic model mice (db/db mice) were intravenously injected with DHI and corresponding virus particles. MiR-30d-5p and JAK1 were detected. The body weight and fasting blood glucose mice were measured every 4 weeks. The renal tissues and serum of mice were collected, and the contents of creatinine and blood urea nitrogen were biochemically analyzed. IL-6, IFN-γ and TNF-α were detected by ELISA, with the pathological conditions of renal tissues in mice by He staining, and the adjustment conditions by TUNEL. Human retinal pigment epithelium (ARPE-19) cells were selected to induce DR model in vitro by high glucose, and exposed to DHI for treatment. The corresponding plasmids were transfected, and miR-30d-5p and JAK1 were detected, with the proliferation ability by plate cloning, apoptosis by flow cytometry, and cell migration ability by Transwell. The angiogenesis ability of cells was assessed by tube formation assay. The targeting relationship between miR-30d-5p and JAK1 was detected. The results manifested that miR-30d-5p was declined in DR and DN, while JAK1 expression was elevated. DHI was able to improve DR and renal injury. DHI could regulate the miR-30d-5p-JAK1 axis in vivo , and miR-30d-5p targeted and regulated JAK1. Upregulation of miR-30d-5p or inhibition of JAK1 could improve DR and renal injury. The results implies that DHI can repress the development of DR and DN by elevating miR-30d-5p and targeting JAK1.

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miR-200-3p suppresses cell proliferation and reduces apoptosis in diabetic retinopathy via blocking the TGF-β2/Smad pathway

Cited by 18 publications

References 38 publications

Hyperoside improves diabetic retinopathy by regulating TGF-β1/miR-200b/VEGF pathway

Hyperoside improves diabetic retinopathy by regulating TGF-β1/miR-200b/VEGF pathway

The Role of miR-29 Family in TGF-β Driven Fibrosis in Glaucomatous Optic Neuropathy

Danhong injection represses diabetic retinopathy and nephropathy advancement in diabetic mice by upregulating microRNA-30d-5p and targeting JAK1

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