Lnc-ing
            <i>NOTCH1</i>
            to Idiopathic Calcific Aortic Valve Disease

Merryman, W. David; Clark, Catherine L.

doi:10.1161/circulationaha.116.025601

Cited by 8 publications

(6 citation statements)

References 15 publications

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“…Wang et al reported the LncRNA TUG1 sponges miR-204-5p to promote osteoblast differentiation through upregulating Runx2 expression in aortic valve calcification [23]. Moreover, Merryman et al found that the lncRNA notch receptor 1 (NOTCH1) is involved in the development of idiopathic calcified aortic valve disease (CAVD) [24]. Zhu et al also reported that downregulation of the lncRNA Angelman syndrome chromosome region (ANCR) promoted osteoblast differentiation by targeting enhancer of zeste 2 polycomb repressive complex 2 subunits (EZH2) and regulating RUNX2 expression [25].…”

Section: Discussionmentioning

confidence: 99%

Genome-wide identification of lncRNAs and mRNAs differentially expressed in human vascular smooth muscle cells stimulated by high phosphorus

et al. 2020

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Background: Cardiovascular events are the primary cause of death for chronic kidney disease patients, which occurred via vascular calcification evolving pathogenically. Although a high level of phosphorus contributes to the induction of osteogenic differentiation of vascular smooth muscle cells (VSMCs), the role of lncRNA in this process awaits further study. Methods: In this study, we systematically investigated the variation of gene expression in human VSMCs induced by high phosphorus. LncRNAs and mRNAs expression were revealed by microarray analyses of the control group and high-phosphorus (HP) group. LncRNA-mRNA co-expression network was established based on the specific lncRNA-mRNA relationships. Hierarchical clustering was used to identify a common set of regulated genes. In addition, Gene Ontology enrichment, Kyoto Gene-Encyclopedia and genomic analyses were conducted for the mRNAs differentially expressed under high phosphorus. Result: RT-qPCR results confirmed that the expression of RUNX2, BMP2 and osteocalcin in HP group exhibited significant increases than in control group (p < .05). VSMC in HP group also showed higher intracellular calcium content. Volcano plots results show that 379 mRNAs and 728 lncRNAs different expressed in HP group. LncRNA-mRNA co-expression networks analysis revealed that 8 lncRNAs were the most highly connected lncRNAs. Quantitative analysis indicated that two lncRNAs were confirmed to increase significantly in the HP group. The mRNA expression of NT5E and ICAM1 were higher in group HP, while MAP3K7CL was lower than CON group (p < .05). Conclusion: This study provided a working list of lncRNAs that may be relevant to osteogenic differentiation, which presents a new insights into the mechanism of vascular calcification induced by high phosphorus in VSMCs.

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Section: Discussionmentioning

confidence: 99%

Genome-wide identification of lncRNAs and mRNAs differentially expressed in human vascular smooth muscle cells stimulated by high phosphorus

et al. 2020

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“…Indeed, miRNA sequences may be embedded into lncRNAs that, in this way, can act as progenitors or reservoirs of miRNAs [14,151]. An example is H19, involved in several CVDs and deregulated under cell stress conditions [119,148,152,153], which is the precursor of miR-675 [154]. In particular, the lncRNA H19 via miR-675 regulates the expression of miR-675 target VDAC1 [155].…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Long Noncoding Competing Endogenous RNA Networks in Age-Associated Cardiovascular Diseases

Greco

Gaetano

Martelli

2019

IJMS

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Cardiovascular diseases (CVDs) are the most serious health problem in the world, displaying high rates of morbidity and mortality. One of the main risk factors for CVDs is age. Indeed, several mechanisms are at play during aging, determining the functional decline of the cardiovascular system. Aging cells and tissues are characterized by diminished autophagy, causing the accumulation of damaged proteins and mitochondria, as well as by increased levels of oxidative stress, apoptosis, senescence and inflammation. These processes can induce a rapid deterioration of cellular quality-control systems. However, the molecular mechanisms of age-associated CVDs are only partially known, hampering the development of novel therapeutic strategies. Evidence has emerged indicating that noncoding RNAs (ncRNAs), such as long ncRNAs (lncRNAs) and micro RNAs (miRNAs), are implicated in most patho-physiological mechanisms. Specifically, lncRNAs can bind miRNAs and act as competing endogenous-RNAs (ceRNAs), therefore modulating the levels of the mRNAs targeted by the sponged miRNA. These complex lncRNA/miRNA/mRNA networks, by regulating autophagy, apoptosis, necrosis, senescence and inflammation, play a crucial role in the development of age-dependent CVDs. In this review, the emerging knowledge on lncRNA/miRNA/mRNA networks will be summarized and the way in which they influence age-related CVDs development will be discussed.

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“…lncRNA NEAT1 has been also shown to be highly expressed in nasopharyngeal cancer and LSCC and can regulate radio‐resistance, proliferation, invasion and apoptosis 25,26 . In addition, some other important lncRNAs (eg, H19 , 27 NOTCH1 , 28 MALAT1 29 and HOTAIR 30 ) were proven to be expressed in both tumors and adjacent tissues. Furthermore, some lncRNAs expressed in laryngeal carcinomas have been studied.…”

Section: Discussionmentioning

confidence: 99%

lncRNA IGKJ2‐MALLP2 suppresses LSCC proliferation, migration, invasion, and angiogenesis by sponging miR‐1911‐3p/p21

Cao

Yang

et al. 2020

Cancer Science

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Because advanced laryngeal squamous cell carcinoma (LSCC) is diagnosed as a malignant tumor with a poor prognosis, the associated mechanisms still need to be further investigated. As key players in the development and progression of LSCC, lncRNAs have attracted increasing attention from many researchers. In this study, a novel lncRNA termed IGKJ2‐MALLP2 was identified and investigated for its effects on the development of LSCC. IGKJ2‐MALLP2 expression was confirmed by RT‐qPCR in 78 pairs of tissues and human laryngeal carcinoma cell lines. The results of this study showed that the expression of IGKJ2‐MALLP2 was reduced in LSCC tissues and displayed close relationships with tumor stage, lymph node metastasis, and clinical stage. Using a dual‐luciferase reporter assay, the ability of miR‐1911‐3p to bind both IGKJ2‐MALLP2 and p21 mRNA was demonstrated. IGKJ2‐MALLP2 could upregulate p21 expression by competitively binding miR‐1911‐3p. Moreover, IGKJ2‐MALLP2 effectively hindered the invasion, migration, and proliferation of AMC‐HN‐8 and TU212 tumor cells. Furthermore, its high expression could hinder the secretion of VEGF‐A and suppress angiogenesis. As revealed by the results of in vitro experiments, IGKJ2‐MALLP2 overexpression could restrict tumor growth and blood vessel formation in a xenograft model of LSCC. As indicated from the mentioned findings, IGKJ2‐MALLP2, which mediates p21 expression by targeting miR‐1911‐3p, was capable of regulating LSCC progression and could act as an underlying therapeutic candidate to treat LSCC.

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Lnc-ing NOTCH1 to Idiopathic Calcific Aortic Valve Disease

Cited by 8 publications

References 15 publications

Genome-wide identification of lncRNAs and mRNAs differentially expressed in human vascular smooth muscle cells stimulated by high phosphorus

Genome-wide identification of lncRNAs and mRNAs differentially expressed in human vascular smooth muscle cells stimulated by high phosphorus

Long Noncoding Competing Endogenous RNA Networks in Age-Associated Cardiovascular Diseases

lncRNA IGKJ2‐MALLP2 suppresses LSCC proliferation, migration, invasion, and angiogenesis by sponging miR‐1911‐3p/p21

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