Long non-coding RNA MALAT1 functions as miR-1 sponge to regulate Connexin 43-mediated ossification of the posterior longitudinal ligament

Yuan, Xiaoqiu; Guo, Yongfei; Chen, Dechun; Luo, Yibin; Chen, Deyu; Miao, Jinhao; Chen, Yu

doi:10.1016/j.bone.2019.06.019

Cited by 31 publications

(29 citation statements)

References 33 publications

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“…The starBase tool ( http://starbase.sysu.edu.cn/agoClipRNA.php?source=lncRNA ) predicted the presence of miR-503 binding sites on lncRNA MALAT1, and the TargetScan tool predicted that the presence of miR-503 binding sites on the TLR4 gene. Several studies have confirmed that lncRNA MALAT1 acts as a “molecular sponge” of microRNA [ 35 , 36 ]. Moreover, lncRNA MALAT1 was shown to act as a “molecular sponge” of miR-124-3p.1, to regulate the expression of KLF5, and to promote the vascular remodeling and cell cycle process of PAH [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Long-Chain Non-Coding RNA Metastasis-Related Lung Adenocarcinoma Transcript 1 (MALAT1) Promotes the Proliferation and Migration of Human Pulmonary Artery Smooth Muscle Cells (hPASMCs) by Regulating the MicroRNA-503 (miR-503)/Toll-Like Receptor 4 (TLR4) Signal Axis

Shen

Zhang

et al. 2020

Med Sci Monit

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Section: Discussionmentioning

confidence: 99%

Long-Chain Non-Coding RNA Metastasis-Related Lung Adenocarcinoma Transcript 1 (MALAT1) Promotes the Proliferation and Migration of Human Pulmonary Artery Smooth Muscle Cells (hPASMCs) by Regulating the MicroRNA-503 (miR-503)/Toll-Like Receptor 4 (TLR4) Signal Axis

Shen

Zhang

et al. 2020

Med Sci Monit

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“…In addition, there is an increase of ZFHX3 expression in HL-1 cells, even not statistically significant, which was caused by 18-α-GA treated to the contractile-like SMCs. It was noticeable that ZFHX3 was a target gene of miR-1 [41], which was reported to be negatively regulated by long non-coding RNA MALAT1 through gap junction connexins such as Cx43 [42]. Then it needs to be explored further whether the inhibition of heterocellular gap junctions by 18-α-GA in SMCs could negatively regulate ZFHX3 expression via the MALAT1-Cx43-miR-1 axis in HL-1 cells.…”

Section: Discussionmentioning

confidence: 99%

Vascular smooth muscle cell phenotypic transition regulates gap junctions of cardiomyocyte

Zhou

Zhang

et al. 2020

Heart Vessels

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Atrial fibrillation (AF) is one of the most prevalent arrhythmias. Myocardial sleeves of the pulmonary vein are critical in the occurrence of AF. Our study aims to investigate the effect of synthetic vascular smooth muscle cells (SMCs) on gap junction proteins in cardiomyocytes. (1) Extraction of vascular SMCs from the pulmonary veins of Norway rats. TGF-β 1 was used to induce the vascular SMCs switching to the synthetic phenotype and 18-α-GA was used to inhibit gap junctions of SMCs. The contractile and synthetic phenotype vascular SMCs were cocultured with HL-1 cells; (2) Western blotting was used to detect the expression of Cx43, Cx40 and Cx45 in HL-1 cells, and RT-PCR to test microRNA 27b in vascular SMCs or in HL-1 cells; (3) Lucifer yellow dye transfer experiment was used to detect the function of gap junctions. (1) TGF-β 1 induced the vascular SMCs switching to synthetic phenotype; (2) Cx43 was significantly increased, and Cx40 and Cx45 were decreased in HL-1 cocultured with synthetic SMCs; (3) The fluorescence intensity of Lucifer yellow was higher in HL-1 cocultured with synthetic SMCs than that in the cells cocultured with contractile SMCs, which was inhibited by18-α-GA; (4) the expression of microRNA 27b was increased in HL-1 cocultured with synthetic SMCs, which was attenuated markedly by 18-α-GA. (5) the expression of ZFHX3 was decreased in HL-1 cocultured with synthetic SMCs, which was reversed by 18-α-GA. The gap junction proteins of HL-1 were regulated by pulmonary venous SMCs undergoing phenotypic transition in this study, accompanied with the up-regulation of microRNA 27b and the down-regulation of ZFHX3 in HL-1 cells, which was associated with heterocellular gap junctions between HL-1 and pulmonary venous SMCs.

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“…In this view, lncRNA H19 has been reported to enhance osteoblast proliferation by sequestering miR-141 and miR-22, negative regulators of osteogenesis and the Wnt/β-catenin pathway [71]. Similarly, lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT 1) acted as miR-1 sponge to inhibit its suppressive transcription effect on Connexin43 [72]. For these reasons, these lncRNAs were defined as competing endogenous RNAs (ceRNAs) ( Figure 1).…”

Section: Long Non-coding Rnas (Lncrnas)mentioning

confidence: 99%

The Role of Extracellular Vesicles (EVs) in the Epigenetic Regulation of Bone Metabolism and Osteoporosis

Muraca

Cappariello

2020

IJMS

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Extracellular vesicles (EVs) are complex phospholipidic structures actively released by cells. EVs are recognized as powerful means of intercellular communication since they contain many signaling molecules (including lipids, proteins, and nucleic acids). In parallel, changes in epigenetic processes can lead to changes in gene function and finally lead to disease onset and progression. Recent breakthroughs have revealed the complex roles of non-coding RNAs (microRNAs (miRNAs) and long non-coding RNAs (lncRNAs)) in epigenetic regulation. Moreover, a substantial body of evidence demonstrates that non-coding RNAs can be shuttled among the cells and tissues via EVs, allowing non-coding RNAs to reach distant cells and exert systemic effects. Resident bone cells, including osteoclasts, osteoblasts, osteocytes, and endothelial cells, are tightly regulated by non-coding RNAs, and many of them can be exported from the cells to neighboring ones through EVs, triggering pathological conditions. For these reasons, researchers have also started to exploit EVs as a theranostic tool to address osteoporosis. In this review, we summarize some recent findings regarding the EVs’ involvement in the fine regulation of non-coding RNAs in the context of bone metabolism and osteoporosis.

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Long non-coding RNA MALAT1 functions as miR-1 sponge to regulate Connexin 43-mediated ossification of the posterior longitudinal ligament

Cited by 31 publications

References 33 publications

Long-Chain Non-Coding RNA Metastasis-Related Lung Adenocarcinoma Transcript 1 (MALAT1) Promotes the Proliferation and Migration of Human Pulmonary Artery Smooth Muscle Cells (hPASMCs) by Regulating the MicroRNA-503 (miR-503)/Toll-Like Receptor 4 (TLR4) Signal Axis

Long-Chain Non-Coding RNA Metastasis-Related Lung Adenocarcinoma Transcript 1 (MALAT1) Promotes the Proliferation and Migration of Human Pulmonary Artery Smooth Muscle Cells (hPASMCs) by Regulating the MicroRNA-503 (miR-503)/Toll-Like Receptor 4 (TLR4) Signal Axis

Vascular smooth muscle cell phenotypic transition regulates gap junctions of cardiomyocyte

The Role of Extracellular Vesicles (EVs) in the Epigenetic Regulation of Bone Metabolism and Osteoporosis

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