Long non-coding RNAs in coronary atherosclerosis

Wang, Yiran; Song, Xianjing; Li, Zhibo; Liu, Bin

doi:10.1016/j.lfs.2018.08.072

Cited by 19 publications

(12 citation statements)

References 112 publications

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“…Long noncoding RNAs (lncRNAs) are RNAs with a length of more than 200 nucleotides [14]. They participate in cell proliferation, autophagy, apoptosis, and senescence [14,15]. An abnormal lncRNA expression is associated with vascular cell dysfunction.…”

Section: Agingmentioning

confidence: 99%

Downregulation of LncRNA NORAD promotes Ox-LDL-induced vascular endothelial cell injury and atherosclerosis

Bian

Jing

Yang

et al. 2020

Aging

120

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Long noncoding RNAs (lncRNAs) play important roles in the development of vascular diseases. However, the effect of lncRNA NORAD on atherosclerosis remains unknown. This study aimed to investigate the effect NORAD on endothelial cell injury and atherosclerosis. Ox-LDL-treated human umbilical vein endothelial cells (HUVECs) and high-fat-diet (HFD)-fed ApoE −/− mice were used as in vitro and in vivo models. Results showed that NORAD-knockdown induced cell cycle arrest in G0/G1 phase, aggravated ox-LDL-induced cell viability reduction, cell apoptosis, and cell senescence along with the increased expression of Bax, P53, P21 and cleaved caspase-3 and the decreased expression of Bcl-2. The effect of NORAD on cell viability was further verified via NORAD-overexpression. NORAD-knockdown increased ox-LDL-induced reactive oxygen species, malondialdehyde, p-IKBα expression levels and NF-κB nuclear translocation. Proinflammatory molecules ICAM, VCAM, and IL-8 were also increased by NORAD-knockdown. Additionally, we identified the strong interaction of NORAD and IL-8 transcription repressor SFPQ in HUVECs. In ApoE −/− mice, NORAD-knockdown increased the lipid disorder and atherosclerotic lesions. The results have suggested that lncRNA NORAD attenuates endothelial cell senescence, endothelial cell apoptosis, and atherosclerosis via NF-κB and p53-p21 signaling pathways and IL-8, in which NORAD-mediated effect on IL-8 might through the direct interaction with SFPQ.

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Section: Agingmentioning

confidence: 99%

Downregulation of LncRNA NORAD promotes Ox-LDL-induced vascular endothelial cell injury and atherosclerosis

Bian

Jing

Yang

et al. 2020

Aging

120

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“…LncRNAs are capable of modulating target DNA, RNA, and proteins at the pre-and posttranscriptional level. An increasing number of studies had demonstrated that lncRNAs played a pivotal role in the regulation of VSMC phenotype, functions, perhaps also in the development of VSMCs-related diseases [90,91]. This chapter described the emerging roles of exosomal lncRNAs in VSMCs proliferation, migration, apoptosis, and calcification.…”

Section: Exosomal Lncrnas and Vsmcs Functionsmentioning

confidence: 99%

Roles and Functions of Exosomal Non-coding RNAs in Vascular Aging

Ni¹,

Lin²,

Zhan³

et al. 2020

Aging and disease

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Aging is a progressive loss of physiological integrity and functionality process which increases susceptibility and mortality to diseases. Vascular aging is a specific type of organic aging. The structure and function changes of endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) are the main cause of vascular aging, which could influence the threshold, process, and severity of vascular related diseases. Accumulating evidences demonstrate that exosomes serve as novel intercellular information communicator between cell to cell by delivering variety biologically active cargos, especially exosomal non-coding RNAs (ncRNAs), which are associated with most of aging-related biological and functional disorders. In this review, we will summerize the emerging roles and mechanisms of exosomal ncRNAs in vascular aging and vascular aging related diseases, focusing on the role of exosomal miRNAs and lncRNAs in regulating the functions of ECs and VSMCs. Moreover, the relationship between the ECs and VSMCs linked by exosomes, the potential diagnostic and therapeutic application of exosomes in vascular aging and the clinical evaluation and treatment of vascular aging and vascular aging related diseases will also be discussed.

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“…Long noncoding RNAs (lncRNAs) are RNAs that lack the ability of protein coding and their length are more than 200 nucleotides [12]. In recent years, numerous studies have demonstrated that lncRNAs play a very important role in cell proliferation, osteogenic differentiation, apoptosis, and autophagy [13][14][15]. LncRNA NORAD, as a long noncoding RNA activated by DNA damage, expresses abnormally in many kinds of tumors and serves as an oncogene [16][17][18].…”

Section: Introductionmentioning

confidence: 99%

LncRNA NORAD promotes bone marrow stem cell differentiation and proliferation by targeting miR-26a-5p in steroid-induced osteonecrosis of the femoral head

Yang

et al. 2021

Stem Cell Res Ther

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Background Steroid-induced osteonecrosis of the femoral head (SONFH) is a devastating orthopedic disease, which seriously affects the quality of life of patients. The study aims to investigate the effects of LncRNA NORAD on SONFH. Methods Human bone marrow-derived mesenchymal stem cells (hBMSCs) were isolated from the proximal femur of patients during routine orthopedic surgery and then cultured with dexamethasone (Dex) and transfected with NORAD overexpression vector, siRNA-NORAD and miR-26a-5p mimics. The mRNA expression of NORAD, miR-26a-5p, OPG, RANK, and RANKL was detected by RT-qPCR. Cell proliferation and apoptosis was measured by CCK-8 assay and flow cytometry, respectively. The protein expression of RUNX2, OPG, RANK, and RANKL was detected by western blot. The dual-luciferase reporter gene assay was performed to confirm the binding between NORAD and miR-26a-5p. Results NORAD expression was downregulated in SONFH tissues, while miR-26a-5p expression was upregulated. Overexpression of NORAD improved DEX-induced inhibition of proliferation and differentiation, and promotion of apoptosis in hBMSCs, while knockdown of NORAD led to the opposite results. Moreover, NORAD improved DEX-induced inhibition of proliferation and differentiation, and promotion of apoptosis by regulation of miR-26a-5p in hBMSCs. Conclusions NORAD expression was downregulated in SONFH tissues, while miR-26a-5p expression was upregulated. NORAD improved DEX-induced inhibition of proliferation and differentiation, and promotion of apoptosis by regulation of miR-26a-5p in hBMSCs.

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Long non-coding RNAs in coronary atherosclerosis

Cited by 19 publications

References 112 publications

Downregulation of LncRNA NORAD promotes Ox-LDL-induced vascular endothelial cell injury and atherosclerosis

Downregulation of LncRNA NORAD promotes Ox-LDL-induced vascular endothelial cell injury and atherosclerosis

Roles and Functions of Exosomal Non-coding RNAs in Vascular Aging

LncRNA NORAD promotes bone marrow stem cell differentiation and proliferation by targeting miR-26a-5p in steroid-induced osteonecrosis of the femoral head

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