Noncoding RNAs in Vascular Aging

Cao, Qidong; Wu, Jiu-Ping; Wang, Xiaoli; Song, Chunli

doi:10.1155/2020/7914957

Cited by 29 publications

(19 citation statements)

References 126 publications

(124 reference statements)

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“…LncRNAs have been demonstrated to possess important functions in various biological processes, such as epigenetic modulation, transcriptional and post-transcriptional regulation ( Feng et al, 2006 ; Wang et al, 2016 ). It has been reported that lncRNAs participate in the regulation of cell senescence ( Azzalin et al, 2007 ; Abdelmohsen et al, 2013 ; Cao et al, 2020 ). MALAT1 and MIAT, known as the best-annotated lncRNAs, exhibit lower expression levels in senescent WI-38 cells.…”

Section: Discussionmentioning

confidence: 99%

LncRNA-H19 Drives Cardiomyocyte Senescence by Targeting miR-19a/socs1/p53 Axis

Zhuang

Hongwen

et al. 2021

Front. Pharmacol.

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Purpose: Cardiomyocyte senescence is associated with a progressive decline in cardiac physiological function and the risk of cardiovascular events. lncRNA H19 (H19), a well-known long noncoding RNA (lncRNA), is involved in the pathophysiological process of multiple cardiovascular disease such as heart failure, cardiac ischemia and fibrosis. However, the role of H19 in cardiomyocyte senescence remains to be further explored.Methods: Senescence-associated β-galactosidases (SA-β-gal) staining was used to detect cardiomyocyte senescence. Western blot, qRT-PCR and luciferase reporter assay were employed to evaluate the role of H19 in cardiomyocyte senescence and its underling molecular mechanism.Results: H19 level was significantly increased in high glucose-induced senescence cardiomyocytes and aged mouse hearts. Overexpression of H19 enhanced the number of SA-β-gal-positive cells, and the expression of senescence-related proteins p53 and p21, whereas H19 knockdown exerted the opposite effects. Mechanistically, H19 was demonstrated as a competing endogenous RNA (ceRNA) for microRNA-19a (miR-19a): H19 overexpression downregulated miR-19a level, while H19 knockdown upregulated miR-19a. The expression of SOSC1 was dramatically increased in senescence cardiomyocytes and aged mouse hearts. Further experiments identified SOCS1 as a downstream target of miR-19a. H19 upregulated SOCS1 expression and activated the p53/p21 pathway by targeting miR-19a, thus promoting the cardiomyocytes senescence.Conclusion: Our results show that H19 is a pro-senescence lncRNA in cardiomyocytes acting as a ceRNA to target the miR-19a/SOCS1/p53/p21 pathway. Our research reveals a molecular mechanism of cardiomyocyte senescence regulation and provides a novel target of the therapy for senescence-associated cardiac diseases.

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Section: Discussionmentioning

confidence: 99%

LncRNA-H19 Drives Cardiomyocyte Senescence by Targeting miR-19a/socs1/p53 Axis

Zhuang

Hongwen

et al. 2021

Front. Pharmacol.

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“…in addition, patients with IS are prone to a hypercoagulable state and advanced fibrinolysis. Most patients have coagulation changes in the clinic, which may lead to adverse events such as thrombosis and infarction, which affects the prognosis (50).…”

Section: Discussionmentioning

confidence: 99%

Circulating mRNA and microRNA profiling analysis in patients with ischemic stroke

Sun

Dong

et al. 2020

Mol Med Rep

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To provide insight into molecular diagnosis and individualized treatment of ischemic stroke (iS), several available datasets in iS were analyzed to identify the differentially expressed genes and micrornas (mirnas). Series matrix files from GSE22255 and GSE16561 (mRNA profiles), a well as GSE110993 (miRNA profile) were downloaded from the Gene Expression Omnibus database. System-level clustering was performed with GeneCluster 3.0 software, and gene annotation and pathway enrichment were performed with gene ontology analysis and database for annotation, Visualization and integrated discovery software. For a protein-protein interaction (PPI) network, Biological General Repository for interaction datasets and intact interaction information were integrated to determine the interaction of differentially expressed genes. The selected mirna candidates were imported into the TargetScan, mirdB and mirecords databases for the prediction of target genes. The present study identified 128 upregulated and 231 downregulated genes in female stroke patients, and 604 upregulated and 337 downregulated genes in male stroke patients compared with sex-and age-matched controls. The construction of a PPi network demonstrated that male stroke patients exhibited YWHAE, CUL3 and JUN as network center nodes, and in female patients CYLD, FOS and PIK3R1 interactions were the strongest. notably, these interactions are mainly involved in immune inflammatory response, apoptosis and other biological pathways, such as blood coagulation. Female and male upregulated genes were cross-validated with another set of Illumina HumanRef-8 v3.0 expression beadchip (GSE16561). Functional item association networks, gene function networks and transcriptional regulatory networks were successfully constructed, and the relationships between mirnas and target genes were successfully predicted. The present study identified a number of transcription factors, including DEFA1, PDK4, SDPR, TCN1 and MMP9, and miRNAs, including miRNA (miR)-21, miR-143/145, miR-125-5p and miR-122, which may serve important roles in the development of cerebral stroke and may be important molecular indicators for the treatment of iS.

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“…In this review, we have focused on their role in VSMCs. However, there is also a large body of literature documenting their important roles in regulating endothelial cell function (Wei et al, 2013 ; Cao et al, 2020 ). Thus, an important next step in this field will be to assess whether manipulating miRNA levels in VSMCs selectively is sufficient to induce or prevent arterial stiffening or whether parallel processes in endothelial cells or other cells present in large vessels, such as immune cells or fibroblasts, also play a key role in the pathophysiology of LAS.…”

Section: Summary and Future Directionsmentioning

confidence: 99%

Deciphering the Role of microRNAs in Large-Artery Stiffness Associated With Aging: Focus on miR-181b

et al. 2021

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Large artery stiffness (LAS) is a major, independent risk factor underlying cardiovascular disease that increases with aging. The emergence of microRNA signaling as a key regulator of vascular structure and function has stimulated interest in assessing its role in the pathophysiology of LAS. Identification of several microRNAs that display age-associated changes in expression in aorta has focused attention on defining their molecular targets and deciphering their role in age-associated arterial stiffening. Inactivation of the microRNA-degrading enzyme, translin/trax, which reverses the age-dependent decline in miR-181b, confers protection from aging-associated arterial stiffening, suggesting that inhibitors targeting this enzyme may have translational potential. As LAS poses a major public health challenge, we anticipate that future studies based on these advances will yield innovative strategies to combat aging-associated arterial stiffening.

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Noncoding RNAs in Vascular Aging

Cited by 29 publications

References 126 publications

LncRNA-H19 Drives Cardiomyocyte Senescence by Targeting miR-19a/socs1/p53 Axis

LncRNA-H19 Drives Cardiomyocyte Senescence by Targeting miR-19a/socs1/p53 Axis

Circulating mRNA and microRNA profiling analysis in patients with ischemic stroke

Deciphering the Role of microRNAs in Large-Artery Stiffness Associated With Aging: Focus on miR-181b

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