The long non-coding RNA MALAT1 activates Nrf2 signaling to protect human umbilical vein endothelial cells from hydrogen peroxide

Zeng, Rong; Zhang, Rui; Song, Xiaojing; Ni, Leng; Lai, Zhichao; Liu, Changwei; Ye, Wei

doi:10.1016/j.bbrc.2017.12.105

Cited by 64 publications

(39 citation statements)

References 37 publications

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“…H 2 O 2 induced oxidative injury of ECs and up‐regulated the expression of MALAT1. MALAT1 inhibited apoptosis of HUVECs by activating Nrf2 signaling pathway via down‐regulation of Keap1 . Inflammation cytokines also induce the oxidative injury of ECs.…”

Section: Malat1 and Vascular Diseasesmentioning

confidence: 99%

“…More and more studies have showed that lncRNAs are involved in development of CVDs. Among them, metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) is attracted more attention as it is profoundly expressed in ECs or cardiomyocytes under the conditions of hypoxia, high glucose, cytokines, and oxidative stress, which are the risk factors of CVD . Furthermore, MALAT1 was also found to regulate multiple pathophysiological processes such as proliferation, apoptosis, autophagy, and pyroptosis in ECs or cardiomyocytes …”

Section: Introductionmentioning

confidence: 99%

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The role of lncRNA MALAT1 in cardiovascular disease

Yan

Song

et al. 2019

IUBMB Life

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Cardiovascular disease (CVD) is the first leading cause of death worldwide. Understanding the molecular mechanism of signaling pathways involved in pathology of CVD is benefit for targeted therapeutics. Recently, long non‐coding RNAs (lncRNAs) are found and involved in regulation of pathology of CVD at different levels. Among them, MALAT1 attracted more attention as it was profoundly expressed in endothelial cells or cardiomyocytes in response to the risk factors of CVD, such as hypoxia, high glucose, cytokine, and oxidative stress. In this review, we summarize recent progresses in research on the molecular mechanism of MALAT1 on regulating the pathophysiological processes of CVD as well as its potential therapeutic applications.

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Section: Malat1 and Vascular Diseasesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The role of lncRNA MALAT1 in cardiovascular disease

Yan

Song

et al. 2019

IUBMB Life

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“…Furthermore, it interacts with serine/arginine-rich proteins to regulate the subcellular localization of splicing regulatory proteins [21]. Recent studies have proposed the pro-survival function of Lnc-MALAT1 [22]. However, the potential activity of Lnc-MALAT1 in Dex-treated human osteoblasts has not yet been studied.…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, Lnc-MALAT1 could provoke AMPK-dependent antioxidant mechanisms to protect human osteoblasts from Dex-induced injury [22].…”

Section: Cellular Physiology and Biochemistry Cellular Physiology Andmentioning

confidence: 99%

Long Non-Coding RNA MALAT1 Protects Human Osteoblasts from Dexamethasone-Induced Injury via Activation of PPM1E-AMPK Signaling

Fan¹,

Zhang²,

Liu³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Dexamethasone (Dex) induces injuries to human osteoblasts. In this study, we tested the potential role of the long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (Lnc-MALAT1) in this process. Materials: Two established human osteoblastic cell lines (OB-6 and hFOB1.19) and primary human osteoblasts were treated with Dex. Lnc-MALAT1 expression was analyzed by quantitative real-time polymerase chain reaction assay. Cell viability, apoptosis, and death were tested by the MTT assay, histone-DNA assay, and trypan blue staining assay, respectively. AMP-activated protein kinase (AMPK) signaling was evaluated by western blotting and AMPK activity assay. Results: Lnc-MALAT1 expression was downregulated by Dex treatment in the established osteoblastic cell lines (OB-6 and hFOB1.19) and primary human osteoblasts. The level of Lnc-MALAT1 was decreased in the necrotic femoral head tissues of Dex-administered patients. In osteoblastic cells and primary human osteoblasts, forced overexpression of Lnc-MALAT1 using a lentiviral vector (LV-MALAT1) inhibited Dex-induced cell viability reduction, cell death, and apoptosis. Conversely, transfection with Lnc-MALAT1 small interfering RNA aggravated Dex-induced cytotoxicity. Transfection with LV-MALAT1 downregulated Ppm1e (protein phosphatase, Mg^2+/ Mn²⁺-dependent 1e) expression to activate AMPK signaling. Treatment of osteoblasts with AMPKα1 short hairpin RNA or dominant negative mutation (T172A) abolished LV-MALAT1-induced protection against Dex-induced cytotoxicity. Furthermore, LV-MALAT1 induced an increase in nicotinamide adenine dinucleotide phosphate activity and activation of Nrf2 signaling. Dex-induced reactive oxygen species production was significantly attenuated by LV-MALAT1 transfection in osteoblastic cells and primary osteoblasts. Conclusion: Lnc-MALAT1 protects human osteoblasts from Dex-induced injuries, possibly via activation of Ppm1e-AMPK signaling.

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“…As reported, LncRNA could regulate the target protein mainly by directly binding to the target protein [14]. Thus, to further validate the association between MALAT1 and MARCH7, we performed RNA immunoprecipitation (RIP) assay with an antibody against MARCH7 on SKOV3 cellular extracts.…”

Section: March7 Interaction With Malat1 Depends On Mir-200amentioning

confidence: 99%

Interaction of E3 Ubiquitin Ligase MARCH7 with Long Noncoding RNA MALAT1 and Autophagy-Related Protein ATG7 Promotes Autophagy and Invasion in Ovarian Cancer

Zhang

Mei

et al. 2018

Cell Physiol Biochem

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Background/Aims: Ubiquitin E3 ligase MARCH7 plays an important role in T cell proliferation and neuronal development. But its role in ovarian cancer remains unclear. This study aimed to investigate the role of Ubiquitin E3 ligase MARCH7 in ovarian cancer. Methods: Real-time PCR, immunohistochemistry and western blotting analysis were performed to determine the expression of MARCH7, MALAT1 and ATG7 in ovarian cancer cell lines and clinical specimens. The role of MARCH7 in maintaining ovarian cancer malignant phenotype was examined by Wound healing assay, Matrigel invasion assays and Mouse orthotopic xenograft model. Luciferase reporter assay, western blot analysis and ChIP assay were used to determine whether MARCH7 activates TGF-β-smad2/3 pathway by interacting with TGFβR2. Results: MARCH7 interacted with MALAT1 by miR-200a (microRNA-200a). MARCH7 may function as a competing endogenous RNA (ceRNA) to regulate the expression of ATG7 by competing with miR-200a. MARCH7 regulated TGF-β-smad2/3 pathway by interacting with TGFβR2. Inhibition of TGF-β-smad2/3 pathway downregulated MARCH7, MALAT1 and ATG7. MiR-200a regulated TGF-β induced autophagy, invasion and metastasis of SKOV3 cells by targeting MARCH7. MARCH7 silencing inhibited autophagy invasion and metastasis of SKOV3 cells both in vitro and in vivo. In contrast, MARCH7 overexpression promoted TGF-β induced autophagy, invasion and metastasis of A2780 cells in vitro by depending on MALAT1 and ATG7. We also found that TGF-β-smad2/3 pathway regulated MARCH7 and ATG7 through MALAT1. Conclusions: These findings suggested that TGFβR2-Smad2/3-MALAT1/MARCH7/ATG7 feedback loop mediated autophagy, migration and invasion in ovarian cancer.

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The long non-coding RNA MALAT1 activates Nrf2 signaling to protect human umbilical vein endothelial cells from hydrogen peroxide

Cited by 64 publications

References 37 publications

The role of lncRNA MALAT1 in cardiovascular disease

The role of lncRNA MALAT1 in cardiovascular disease

Long Non-Coding RNA MALAT1 Protects Human Osteoblasts from Dexamethasone-Induced Injury via Activation of PPM1E-AMPK Signaling

Interaction of E3 Ubiquitin Ligase MARCH7 with Long Noncoding RNA MALAT1 and Autophagy-Related Protein ATG7 Promotes Autophagy and Invasion in Ovarian Cancer

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