miRNA-9 inhibits apoptosis and promotes proliferation in angiotensin II-induced human umbilical vein endothelial cells by targeting MDGA2

doi:10.31083/j.rcm.2019.02.514

Cited by 9 publications

(4 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“… 25 MiR‐9 inhibited apoptosis and promoted proliferation in angiotensin II–induced human umbilical vein endothelial cells by targeting MDGA2. 26 Our previous study found that miR‐9 positively regulated NSC differentiation. 13 The current study showed that miR‐9 positively regulated BMEC proliferation and migration and reduced cell death.…”

Section: Discussionmentioning

confidence: 96%

Neural stem cell–derived exosomes regulate cell proliferation, migration, and cell death of brain microvascular endothelial cells via the miR‐9/Hes1 axis under hypoxia

Deng,

Hu,

Wang

et al. 2024

Anim Models and Exp Med

View full text Add to dashboard Cite

BackgroundOur previous study found that mouse embryonic neural stem cell (NSC)–derived exosomes (EXOs) regulated NSC differentiation via the miR‐9/Hes1 axis. However, the effects of EXOs on brain microvascular endothelial cell (BMEC) dysfunction via the miR‐9/Hes1 axis remain unknown. Therefore, the current study aimed to determine the effects of EXOs on BMEC proliferation, migration, and death via the miR‐9/Hes1 axis.MethodsImmunofluorescence, quantitative real‐time polymerase chain reaction, cell counting kit‐8 assay, wound healing assay, calcein‐acetoxymethyl/propidium iodide staining, and hematoxylin and eosin staining were used to determine the role and mechanism of EXOs on BMECs.ResultsEXOs promoted BMEC proliferation and migration and reduced cell death under hypoxic conditions. The overexpression of miR‐9 promoted BMEC proliferation and migration and reduced cell death under hypoxic conditions. Moreover, miR‐9 downregulation inhibited BMEC proliferation and migration and also promoted cell death. Hes1 silencing ameliorated the effect of amtagomiR‐9 on BMEC proliferation and migration and cell death. Hyperemic structures were observed in the regions of the hippocampus and cortex in hypoxia‐induced mice. Meanwhile, EXO treatment improved cerebrovascular alterations.ConclusionNSC‐derived EXOs can promote BMEC proliferation and migration and reduce cell death via the miR‐9/Hes1 axis under hypoxic conditions. Therefore, EXO therapeutic strategies could be considered for hypoxia‐induced vascular injury.

show abstract

Section: Discussionmentioning

confidence: 96%

Neural stem cell–derived exosomes regulate cell proliferation, migration, and cell death of brain microvascular endothelial cells via the miR‐9/Hes1 axis under hypoxia

Deng,

Hu,

Wang

et al. 2024

Anim Models and Exp Med

View full text Add to dashboard Cite

show abstract

“…Second, while many of the uniquely regulated proteins in our data set are not previously linked to angiogenesis, several were reported to regulate endothelial cell function. For example, during vessel regression Mdga2 (Table S6), a protein that promotes apoptosis and inhibits endothelial cell proliferation, was upregulated while Tmem33, which promotes VEGF function and angiogenesis, was downregulated. Similarly, during neovascularization Fibronectin 1 (Fn1) and insulin-like growth factor 2 MRNA-binding protein 3 (IGF2BP3), two factors that promote endothelial cell proliferation and new vessel growth, , were upregulated (Table S7).…”

Section: Discussionmentioning

confidence: 99%

Novel Regulators of Retina Neovascularization: A Proteomics Approach

Jiang

et al. 2021

J. Proteome Res.

View full text Add to dashboard Cite

The purpose of this study was to identify proteins that regulate vascular remodeling in an ROP mouse model. Pups were subjected to fluctuating oxygen levels and retinas sampled during vessel regression (PN12) or neovascularization (PN17) for comparative SWATH-MS proteomics using liquid chromatography-tandem mass spectrometry (LC-MS/MS). We developed a human retinal endothelial cell (HREC) ROP correlate to validate the expression of retina neovascular-specific markers. A total of 5191 proteins were identified in OIR retinas with 498 significantly regulated in elevated oxygen and 345 after a return to normoxia. A total of 122 proteins were uniquely regulated during vessel regression and 69 during neovascularization (FC ≥ 1.5; p ≤ 0.05), with several validated by western blot analyses. Expressions of 56/69 neovascular-specific proteins were confirmed in hypoxic HRECs with 23 regulated in the same direction as OIR neovascular retinas. These proteins control angiogenesis-related processes including matrix remodeling, cell migration, adhesion, and proliferation. RNAi and transfection overexpression studies confirmed that VASP and ECH1, showing the highest levels in hypoxic HRECs, promoted human umbilical vein (HUVEC) and HREC cell proliferation, while SNX1 and CD109, showing the lowest levels, inhibited their proliferation. These proteins are potential biomarkers and exploitable intervention tools for vascular-related disorders. The proteomics data set generated has been deposited to the ProteomeXchange/iProX Consortium with the Identifier:PXD029208.

show abstract

“…There are only a few studies showing the regulatory role of miRNAs in mitochondrial function in hypertension. One of them is the study of Tan et al In their study was demonstrated that miR-9 inhibited expression of MAM (mitochondria associated membrane) domain containing glycosylphosphatidylinositol anchor 2 (MDGA2) leading to the inhibition of apoptosis and promotion of proliferation in angiotensin II-treated human umbilical vein endothelial cells (HUVECs) [ 116 ]. It is known that MDGA2 is a transcription factor and being mitochondria-related gene, and its dysregulation related to several human diseases [ 117 ].…”

Section: Regulation Of Mirnas In Risk Factorsmentioning

confidence: 99%

The Role of Mitochondria-Targeting miRNAs in Intracerebral Hemorrhage

Gareev

Beylerli

Liang

et al. 2023

View full text Add to dashboard Cite

Non-traumatic intracerebral hemorrhage (ICH) is the most common type of hemorrhagic stroke, most often occurring between the ages of 45 and 60. Arterial hypertension (AH) is most often the cause of ICH, followed by atherosclerosis, blood diseases, inflammatory changes in cerebral vessels, intoxication and vitamin deficiencies. Cerebral hemorrhage can occur by diapedesis or as a result of a ruptured vessel. AH is difficult to treat; requires surgery and can lead to disability or death. One of the important directions in the study of the pathogenesis of ICH is mitochondrial dysfunction and its regulation. The key role of mitochondrial dysfunction in AH and atherosclerosis, as well as in the development of brain damage after hemorrhage, has been acknowledged. MicroRNAs (miRNAs) are a class of non-coding RNAs (about 18-22 nucleotides) that regulate a variety of biological processes including cell differentiation, proliferation, apoptosis, etc., primarily through gene repression. There is growing evidence to support dysregulated miRNAs in various cardiovascular diseases, including ICH. Further, the realization of miRNAs within mitochondrial compartment has challenged the traditional knowledge of signaling pathways involved in the regulatory network of cardiovascular diseases. However, the role of miRNAs in mitochondrial dysfunction for ICH is still under-appreciated, with comparatively much lesser studies and investigations reported, than those in other cardiovascular diseases. In this review, we summarize the up-to-date findings on the published role miRNAs in mitochondrial function for ICH, and the potential use of miRNAs in clinical settings, such as potential therapeutic targets and non-invasive diagnostic/prognostic biomarker tools.

show abstract

miRNA-9 inhibits apoptosis and promotes proliferation in angiotensin II-induced human umbilical vein endothelial cells by targeting MDGA2

Cited by 9 publications

References 19 publications

Neural stem cell–derived exosomes regulate cell proliferation, migration, and cell death of brain microvascular endothelial cells via the miR‐9/Hes1 axis under hypoxia

Neural stem cell–derived exosomes regulate cell proliferation, migration, and cell death of brain microvascular endothelial cells via the miR‐9/Hes1 axis under hypoxia

Novel Regulators of Retina Neovascularization: A Proteomics Approach

The Role of Mitochondria-Targeting miRNAs in Intracerebral Hemorrhage

Contact Info

Product

Resources

About