MiR-191 inhibit angiogenesis after acute ischemic stroke targeting VEZF1

Du, Kang; Zhao, Can; Wang, Li; Wang, Yue; Zhang, Kang-Zhen; Shen, Xi-Yu; Sun, Hui-Xian; Gao, Wei; Lü, Xiang

doi:10.18632/aging.101948

Cited by 62 publications

(31 citation statements)

References 52 publications

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“…The expressions of MV markers (CD63 and CD9) were detected, and the results showed that the isolation was successful ( Figure 1B). Meanwhile, miRNAs including let-7a-5p, 28 miR-103a-3p, 29 miR-191-5p, 30 and miR-26a-5p 31 have been reported to be related to cell apoptosis, proliferation, migration, and angiogenesis of HUVECs. Therefore, the expressions of let-7a-5p, miR-103a-3p, miR-191-5p, miR-377, and miR-26a-5p were compared in CC-MVs with or without interfering E6/E7.…”

Section: Mir-377 Was Increased In E6/ E7-interfering Cc-mvsmentioning

confidence: 99%

<p>Interfering Human Papillomavirus E6/E7 Oncogenes in Cervical Cancer Cells Inhibits the Angiogenesis of Vascular Endothelial Cells via Increasing miR-377 in Cervical Cancer Cell-Derived Microvesicles</p>

Zhang¹,

Liu

Guo

et al. 2020

OTT

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Background: The dysregulation of the human papillomavirus 18 E6 and E7 oncogenes plays a critical role in the angiogenesis of cervical cancer (CC), including the proliferation, migration, and tube formation of vascular endothelial cells. Interfering E6/E7 increases the number of CC cell-derived microvesicles (CC-MVs). Additionally, microRNAs (miRNAs) can modulate CC angiogenesis and can be encapsulated in MVs. Objective: We aim to investigate whether E6/E7 affects CC angiogenesis via regulating miRNAs in CC-MVs. Methods: CC-MVs were isolated from a CC cell line (HeLa) which were transfected with small interfering RNAs (siRNAs) against E6/E7 or co-transfected with miR-377 mimics/ inhibitors. The expression of several miRNAs in CC-MVs was detected using quantitative real-time PCR. After co-incubating CC-MVs with human umbilical vein endothelial cells (HUVECs), cell proliferation, migration, and tube formation of HUVECs were determined using cell counting kit-8, transwell, and tube formation assays, respectively. Results: MiR-377 was increased in E6/E7-interfering CC-MVs. Overexpressing miR-377 in CC-MVs suppressed HUVEC proliferation, migration, and tube formation. LPAR2, the cell surface G protein-coupled receptor, was the downstream target of miR-377 in HUVECs. The co-transfection of E6/E7 siRNAs and miR-377 inhibitors in CCs negated the effect of E6/E7 siRNAs on the elevation of miR-377 in CC-MVs. In HUVECs, the co-transfection of E6/E7 siRNAs and miR-377 inhibitors restored the LPAR2 expression which was reduced by the E6/E7 siRNA transfection. Meanwhile, miR-377 mimic reduced LPAR2 expression and inhibited HUVEC proliferation, migration, and tube formation, while such response was negated by LPAR2 overexpression. Conclusion: Interfering E6/E7 increased miR-377 in CC-MVs, and overexpressing miR-377 in CC-MVs inhibited angiogenesis of HUVECs via reducing LPAR2.

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Section: Mir-377 Was Increased In E6/ E7-interfering Cc-mvsmentioning

confidence: 99%

<p>Interfering Human Papillomavirus E6/E7 Oncogenes in Cervical Cancer Cells Inhibits the Angiogenesis of Vascular Endothelial Cells via Increasing miR-377 in Cervical Cancer Cell-Derived Microvesicles</p>

Zhang¹,

Liu

Guo

et al. 2020

OTT

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“…Let-7d induces cellular apoptosis and suppresses the proliferation, migration, and tubulogenesis of ECs ( Ji et al, 2019 ). MiR-125a and miR-191 also promote cell apoptosis and suppress angiogenesis ( Svensson et al, 2014 ; Gu et al, 2017 ; Du et al, 2019 ). These evidences suggest that EC-EVs and their miRNAs are involved in COPD pathogenesis and disease progression.…”

Section: Endothelial Cell-derived Evs In Chronic Obstructive Pulmonarmentioning

confidence: 99%

Intercellular Communication by Vascular Endothelial Cell-Derived Extracellular Vesicles and Their MicroRNAs in Respiratory Diseases

Fujimoto

Fujita

Kadota

et al. 2021

Front. Mol. Biosci.

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Respiratory diseases and their comorbidities, such as cardiovascular disease and muscle atrophy, have been increasing in the world. Extracellular vesicles (EVs), which include exosomes and microvesicles, are released from almost all cell types and play crucial roles in intercellular communication, both in the regulation of homeostasis and the pathogenesis of various diseases. Exosomes are of endosomal origin and range in size from 50 to 150 nm in diameter, while microvesicles are generated by the direct outward budding of the plasma membrane in size ranges of 100–2,000 nm in diameter. EVs can contain various proteins, metabolites, and nucleic acids, such as mRNA, non-coding RNA species, and DNA fragments. In addition, these nucleic acids in EVs can be functional in recipient cells through EV cargo. The endothelium is a distributed organ of considerable biological importance, and disrupted endothelial function is involved in the pathogenesis of respiratory diseases such as chronic obstructive pulmonary disease, pulmonary hypertension, and acute respiratory distress syndrome. Endothelial cell-derived EVs (EC-EVs) play crucial roles in both physiological and pathological conditions by traveling to distant sites through systemic circulation. This review summarizes the pathological roles of vascular microRNAs contained in EC-EVs in respiratory diseases, mainly focusing on chronic obstructive pulmonary disease, pulmonary hypertension, and acute respiratory distress syndrome. Furthermore, this review discusses the potential clinical usefulness of EC-EVs as therapeutic agents in respiratory diseases.

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“…Cerebral miRNA profiles are reportedly significantly altered and affect disease outcomes in central nervous system (CNS) diseases, which has led to an explosion of potential biomarkers for these diseases ( 12 , 13 ). miRNAs associated with the regulation of apoptosis and autophagy during ischemic stroke have been identified ( 14 , 15 ). miRNA binding sites in the coding sequences (CDSs) of mRNAs have been predicted by combining computational approaches and human mRNA expression data ( 16 ).…”

Section: Introductionmentioning

confidence: 99%

miR‑187‑3p inhibitor attenuates cerebral ischemia/reperfusion injury by regulating Seipin‑mediated autophagic flux

Ren

Xie

et al. 2020

Int J Mol Med

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MicroRNAs (miRNAs/miRs) have been reported to affect ischemia/reperfusion (I/R)-induced cerebral damage. miRNAs cause post-transcriptional gene silencing by binding to the protein-coding sequence (CDS) of mRNAs. Seipin has a potential role in regulating autophagic flux. The present study investigated the involvement of miR-187-3p in Seipin expression, autophagic flux and apoptosis in vitro , as well as the underlying mechanism, using PC12 cells exposed to oxygen-glucose deprivation/reoxygenation (OGD/R), which mimicked the process of I/R. In comparison with control PC12 cells, OGD/R caused an increase in the level of miR-187-3p and a decrease in Seipin protein levels without changes in the level of Seipin mRNA. Using bioinformatics analysis, it was identified that miR-187-3p could bind to the CDS of Seipin. miR-187-3p inhibitor attenuated the reduction in Seipin protein expression in OGD/R-treated PC12 cells. Following OGD/R, autophagic flux was reduced and apoptosis was enhanced, which were attenuated by inhibition of miR-187-3p. Compared with OGD/R-treated PC12 cells, Seipin knockdown further impaired autophagic flux and promoted neuronal apoptosis, which were insensitive to inhibition of miR-187-3p. Furthermore, treatment with miR-187-3p inhibitor could decrease the infarction volume in a rat model of middle cerebral artery occlusion/reperfusion. The present findings indicated that miR-187-3p inhibitor attenuated ischemia-induced cerebral damage by rescuing Seipin expression to improve autophagic flux.

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MiR-191 inhibit angiogenesis after acute ischemic stroke targeting VEZF1

Cited by 62 publications

References 52 publications

<p>Interfering Human Papillomavirus E6/E7 Oncogenes in Cervical Cancer Cells Inhibits the Angiogenesis of Vascular Endothelial Cells via Increasing miR-377 in Cervical Cancer Cell-Derived Microvesicles</p>

<p>Interfering Human Papillomavirus E6/E7 Oncogenes in Cervical Cancer Cells Inhibits the Angiogenesis of Vascular Endothelial Cells via Increasing miR-377 in Cervical Cancer Cell-Derived Microvesicles</p>

Intercellular Communication by Vascular Endothelial Cell-Derived Extracellular Vesicles and Their MicroRNAs in Respiratory Diseases

miR‑187‑3p inhibitor attenuates cerebral ischemia/reperfusion injury by regulating Seipin‑mediated autophagic flux

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