Roles of miRNA-24 in regulating endothelial nitric oxide synthase expression and vascular endothelial cell proliferation

Zhang, Wenyu; Yan, Limei; Li, Yumei; Chen, Wei; Hu, Nan; Wang, Hui; Ou, Hesheng

doi:10.1007/s11010-015-2418-y

Cited by 32 publications

(29 citation statements)

References 23 publications

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“…The luciferase reporter assay method was performed as described preciously [29]. The 3'-untranslated regions (UTR) of Smad3 containing the wild or mutated miR-424-5p binding sequences were synthesized by Genescript (Nanjing, China).…”

Section: Methodsmentioning

confidence: 99%

miR-424-5p promotes proliferation of gastric cancer by targeting Smad3 through TGF-β signaling pathway

Wei

et al. 2016

Oncotarget

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MiRNAs have been reported to regulate gene expression and be associated with cancer progression. Recently, miR-424-5p was reported to play important role in a variety of tumors. However, the role and molecular mechanisms of miR-424-5p in GC (gastric cancer) remains largely unknown. In this study, we aimed to explore the role of miR-424-5p in GC. QRT-PCR was used to determine the expression levels of miR-424-5p and Smad3. CCK8 assay, plate clone assay and cell cycle assay were used to measure the effects of miR-424-5p on GC cell proliferation. Luciferase reporter assay and western blotting were used to prove that Smad3 was one of the direct targets of miR-424-5p. Tumorigenesis assay was used to investigate the role of miR-424-5p in tumor growth of GC cells in vivo. We found that miR-424-5p was up-regulated in GC tissues and cells. Over-expression of miR-424-5p could promote the proliferation of GC cells. In addition, luciferase reporter assay and western blotting assay revealed that Smad3 was a direct target of miR-424-5p. Over-expression of Smad3 could partially reverse the effects of miR-424-5p on GC cell proliferation. Our study further revealed that miR-424-5p could inhibit TGF-β signaling pathway by Smad3.

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Section: Methodsmentioning

confidence: 99%

miR-424-5p promotes proliferation of gastric cancer by targeting Smad3 through TGF-β signaling pathway

Wei

et al. 2016

Oncotarget

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“…In addition, miR-101 can induce cell cycle arrest at the G1/S transition and suppress mTOR expression and EC proliferation induced by laminar shear stress [40]. HUVEC proliferation is significantly inhibited by miR-125a and miR-24 via regulation of the expression of Bcl-2 and Sp1, respectively [38, 41]. …”

Section: Mirnas and Vascular Agingmentioning

confidence: 99%

Function, Role, and Clinical Application of MicroRNAs in Vascular Aging

Lin

Zhan

Wang

et al. 2016

BioMed Research International

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Vascular aging, a specific type of organic aging, is related to age-dependent changes in the vasculature, including atherosclerotic plaques, arterial stiffness, fibrosis, and increased intimal thickening. Vascular aging could influence the threshold, process, and severity of various cardiovascular diseases, thus making it one of the most important risk factors in the high mortality of cardiovascular diseases. As endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) are the main cell biological basis of these pathology changes of the vasculature, the structure and function of ECs and VSMCs play a key role in vascular aging. MicroRNAs (miRNAs), small noncoding RNAs, have been shown to regulate the expression of multiple messenger RNAs (mRNAs) posttranscriptionally, contributing to many crucial aspects of cell biology. Recently, miRNAs with functions associated with aging or aging-related diseases have been studied. In this review, we will summarize the reported role of miRNAs in the process of vascular aging with special emphasis on EC and VSMC functions. In addition, the potential application of miRNAs to clinical practice for the diagnosis and treatment of cardiovascular diseases will also be discussed.

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“…Despite the fact that inhibiting miRNAs function (through DICER silencing [25]) prevents NOS3 down-regulation during hypoxia, only four miRNAs that directly affect NOS3 expression have been identified that include miR-214 [72], miR-155 [73], miR-24 [74] and miR-765 [25]. …”

Section: Micrornas - Regulation Of No Productionmentioning

confidence: 99%

“…Direct binding of miR-24 to NOS3 mRNA was confirmed in HUVECs and resulted in lowering eNOS protein levels in normoxia [74]. Although independent studies reported miR-24 induction during hypoxia in human neuroblastoma cells [76], the expression profile of this miRNA during hypoxia in human endothelium requires further study.…”

Section: Micrornas - Regulation Of No Productionmentioning

confidence: 99%

Posttranscriptional and transcriptional regulation of endothelial nitric-oxide synthase during hypoxia: the role of microRNAs

et al. 2016

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Understanding the cellular pathways that regulate endothelial nitric oxide (eNOS, NOS3) expression and consequently nitric oxide (NO) bioavailability during hypoxia is a necessary aspect in the development of novel treatments for cardiovascular disorders. eNOS expression and eNOS-dependent NO cellular signaling during hypoxia promote an equilibrium of transcriptional and posttranscriptional molecular mechanisms that belong to both proapoptotic and survival pathways. Furthermore, NO bioavailability results not only from eNOS levels, but also relies on the presence of eNOS substrate and cofactors, the phosphorylation status of eNOS, and the presence of reactive oxygen species (ROS) that can inactivate eNOS. Since both NOS3 levels and these signaling pathways can also be a subject of posttranscriptional modulation by microRNAs (miRNAs), this class of short noncoding RNAs contribute another level of regulation for NO bioavailability. As miRNA antagomirs or specific target protectors could be used in therapeutic approaches to regulate NO levels, either by changing NOS3 mRNA stability or through factors governing eNOS activity, it is critical to understand their role in governing eNOS activity during hypoxa. In contrast to a large number of miRNAs reported to the change eNOS expression during hypoxia, only a few miRNAs modulate eNOS activity. Furthermore, impaired miRNA biogenesis leads to NOS3 mRNA stabilization under hypoxia. Here we discuss the recent studies that define miRNAs’ role in maintaining endothelial NO bioavailability emphasizing those miRNAs that directly modulate NOS3 expression or eNOS activity.

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Roles of miRNA-24 in regulating endothelial nitric oxide synthase expression and vascular endothelial cell proliferation

Cited by 32 publications

References 23 publications

miR-424-5p promotes proliferation of gastric cancer by targeting Smad3 through TGF-β signaling pathway

miR-424-5p promotes proliferation of gastric cancer by targeting Smad3 through TGF-β signaling pathway

Function, Role, and Clinical Application of MicroRNAs in Vascular Aging

Posttranscriptional and transcriptional regulation of endothelial nitric-oxide synthase during hypoxia: the role of microRNAs

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