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血浆来源的细胞外囊泡通过miR-30b依赖机制对血管生成及随后的增殖性糖尿病视网膜病变的影响。

Effect of plasma-derived extracellular vesicles on angiogenesis and the ensuing proliferative diabetic retinopathy through a miR-30b-dependent mechanism.

作者信息

Wang Ping, Li Chengqian, Deng Yujie, Yu Qing, Meng Xuxia, Jiang Tao, Wang Qing, Fu Yudong

机构信息

Department of Endocrinology, The Affiliated Hospital of Qingdao University, Qingdao, 266003, People's Republic of China.

Department of Ophthalmology, The Affiliated Hospital of Qingdao University, No. 16, Jiangsu Road, Qingdao, 266003, Shandong, People's Republic of China.

出版信息

Diabetol Metab Syndr. 2022 Dec 10;14(1):188. doi: 10.1186/s13098-022-00937-3.

DOI:10.1186/s13098-022-00937-3
PMID:36494734
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9738026/
Abstract

BACKGROUND/PURPOSE: Proliferative diabetic retinopathy (PDR) is a major diabetic microvascular complication, characterized by pathological angiogenesis. This study sets out to investigate the potential molecular mechanism in the angiogenesis during PDR. METHODS: The expression of microRNA-30b (miR-30b) was quantified in a streptozotocin (STZ)-induced mouse model of PDR. The binding affinity between SIRT1 and miR-30b was then identified and validated. After transduction with In-miR-30b or combined with sh-SIRT1, high-glucose (HG)-induced retinal microvascular endothelial cells (RMECs) were co-cultured with extracellular vesicles (EVs) derived from the plasma of PDR mice (plasma-EVs). The proliferation and angiogenesis of RMECs were then detected in vitro. RESULTS: miR-30b expression was upregulated in the retinal tissue of PDR mice. SIRT1 was a target gene of miR-30b and under the negative regulation by miR-30b in RMECs. In contrast, inhibition of miR-30b resulted in elevated SIRT1 expression, thus alleviating the angiogenesis of RMECs. miR-30b was enriched in the plasma-EVs and could be delivered to RMECs, in which miR-30b exerted pro-angiogenic effects. Furthermore, inhibition of miR-30b arrested the progression of PDR in mice by promoting the expression of SIRT1. CONCLUSION: Collectively, the present study pinpointed the involvement of miR-30b delivered by plasma-EVs in PDR angiogenesis, thus laying the basis for the development of novel therapeutic targets for the treatment of PDR.

摘要

背景/目的：增殖性糖尿病视网膜病变（PDR）是一种主要的糖尿病微血管并发症，其特征为病理性血管生成。本研究旨在探究PDR血管生成过程中的潜在分子机制。 方法：在链脲佐菌素（STZ）诱导的PDR小鼠模型中定量检测微小RNA-30b（miR-30b）的表达。随后鉴定并验证沉默信息调节因子1（SIRT1）与miR-30b之间的结合亲和力。用In-miR-30b转导或与sh-SIRT1联合后，将高糖（HG）诱导的视网膜微血管内皮细胞（RMECs）与来自PDR小鼠血浆的细胞外囊泡（EVs）（血浆-EVs）共培养。然后在体外检测RMECs的增殖和血管生成。 结果：PDR小鼠视网膜组织中miR-30b表达上调。SIRT1是miR-30b的靶基因，在RMECs中受miR-30b的负调控。相反，抑制miR-30b导致SIRT1表达升高，从而减轻RMECs的血管生成。miR-30b在血浆-EVs中富集，并可传递至RMECs，其中miR-30b发挥促血管生成作用。此外，抑制miR-30b可通过促进SIRT1的表达阻止小鼠PDR的进展。 结论：总体而言，本研究明确了血浆-EVs传递的miR-30b参与PDR血管生成，从而为开发治疗PDR的新型治疗靶点奠定了基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bbe/9738026/a1dd4b3fae71/13098_2022_937_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bbe/9738026/14c3ed5f286f/13098_2022_937_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bbe/9738026/11be6675eb29/13098_2022_937_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bbe/9738026/3138ddf84b15/13098_2022_937_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bbe/9738026/38b065ba2173/13098_2022_937_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bbe/9738026/ac20f2db9789/13098_2022_937_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bbe/9738026/a1dd4b3fae71/13098_2022_937_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bbe/9738026/14c3ed5f286f/13098_2022_937_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bbe/9738026/11be6675eb29/13098_2022_937_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bbe/9738026/3138ddf84b15/13098_2022_937_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bbe/9738026/38b065ba2173/13098_2022_937_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bbe/9738026/ac20f2db9789/13098_2022_937_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7bbe/9738026/a1dd4b3fae71/13098_2022_937_Fig6_HTML.jpg

相似文献

[1]
Effect of plasma-derived extracellular vesicles on angiogenesis and the ensuing proliferative diabetic retinopathy through a miR-30b-dependent mechanism.

Diabetol Metab Syndr. 2022-12-10

[2]
Functional analysis of miR-21-3p, miR-30b-5p and miR-150-5p shuttled by extracellular vesicles from diabetic subjects reveals their association with diabetic retinopathy.

Exp Eye Res. 2019-4-16

[3]
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Exp Eye Res. 2018-7-3

[4]
Extracellular vesicle-associated microRNA-30b-5p activates macrophages through the SIRT1/ NF-κB pathway in cell senescence.

Front Immunol. 2022

[5]
Overexpression of histone deacetylase SIRT1 exerts an antiangiogenic role in diabetic retinopathy via miR-20a elevation and YAP/HIF1α/VEGFA depletion.

Am J Physiol Endocrinol Metab. 2020-8-10

[6]
MiR-203a-3p inhibits retinal angiogenesis and alleviates proliferative diabetic retinopathy in oxygen-induced retinopathy (OIR) rat model via targeting VEGFA and HIF-1α.

Clin Exp Pharmacol Physiol. 2020-1

[7]
MicroRNA-15b Targets VEGF and Inhibits Angiogenesis in Proliferative Diabetic Retinopathy.

J Clin Endocrinol Metab. 2020-11-1

[8]
MicroRNA-29b-3p inhibits cell proliferation and angiogenesis by targeting VEGFA and PDGFB in retinal microvascular endothelial cells.

Mol Vis. 2020

[9]
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ESC Heart Fail. 2021-10

[10]
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引用本文的文献

[1]
Rekindling Vision: Innovative Strategies for Treating Retinal Degeneration.

Int J Mol Sci. 2025-4-25

[2]
Cell Type-Specific Extracellular Vesicles and Their Impact on Health and Disease.

Int J Mol Sci. 2024-2-27

[3]
Emerging role of extracellular vesicles in diabetic retinopathy.

Theranostics. 2024

[4]
Advances in Research Related to MicroRNA for Diabetic Retinopathy.

J Diabetes Res. 2024-2-12

本文引用的文献

[1]
LncRNA XIST protects podocyte from high glucose-induced cell injury in diabetic nephropathy by sponging miR-30 and regulating AVEN expression.

Arch Physiol Biochem. 2023-6

[2]
Overexpression of histone deacetylase SIRT1 exerts an antiangiogenic role in diabetic retinopathy via miR-20a elevation and YAP/HIF1α/VEGFA depletion.

Am J Physiol Endocrinol Metab. 2020-8-10

[3]
Silencing circ_0001879 inhibits the proliferation and migration of human retinal microvascular endothelial cells under high-glucose conditions via modulating miR-30-3p.

Gene. 2020-7-25

[4]
Rno-microRNA-30c-5p promotes myocardial ischemia reperfusion injury in rats through activating NF-κB pathway and targeting SIRT1.

BMC Cardiovasc Disord. 2020-5-20

[5]
Extracellular Vesicle-Induced Classical Complement Activation Leads to Retinal Endothelial Cell Damage via MAC Deposition.

Int J Mol Sci. 2020-3-1

[6]
MiR-30a-5p accelerates adipogenesis by negatively regulating Sirtuin 1.

Int J Clin Exp Pathol. 2018-11-1

[7]
Functional analysis of miR-21-3p, miR-30b-5p and miR-150-5p shuttled by extracellular vesicles from diabetic subjects reveals their association with diabetic retinopathy.

Exp Eye Res. 2019-4-16

[8]
MicroRNAs in the Progress of Diabetic Nephropathy: A Systematic Review and Meta-Analysis.

Evid Based Complement Alternat Med. 2019-3-7

[9]
Human vitreous in proliferative diabetic retinopathy: Characterization and translational implications.

Prog Retin Eye Res. 2019-4-2

[10]
Pancreatic kallikrein protects against diabetic retinopathy in KK Cg-A/J and high-fat diet/streptozotocin-induced mouse models of type 2 diabetes.

Diabetologia. 2019-3-5

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