LncRNA-MALAT1 promotes CPC proliferation and migration in hypoxia by up-regulation of JMJD6 via sponging miR-125

Li, Linlin; Wang, Qiuyun; Yuan, Zhize; Chen, Anqing; Liu, Zuyun; Wang, Zhe; Li, Haiqing

doi:10.1016/j.bbrc.2018.03.216

Cited by 27 publications

(23 citation statements)

References 28 publications

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“…Proliferation and migration play an important role in angiogenesis or repair of CVD . MALAT1 was up‐regulated by hypoxia and could promote the proliferation and migration potential of cardiac stem cells (CSCs) and cardiac progenitor cells (CPCs) via sponging miR‐155 or miR‐125, respectively . However, inhibition of MALAT1 induced a characteristic phenotype switching from a proliferative toward a more migratory pattern loss in vascular smooth muscle cells (VSMCs) and lead to significant cell cycle arrest in the G2 phase .…”

Section: Malat1 and Pathophysiology Of Cvdsmentioning

confidence: 99%

“…Stem cells have great potential in cardiac regeneration and hold promising therapeutic effect for CVD . Hypoxia could promote the proliferation and migration of CSCs or CPCs accompanied by up‐regulation of MALAT1 . MALAT1 enhanced proliferation and migration potential of CSCs via sponging the miR‐155 targeting myocyte enhancer factor 2A .…”

Section: Malat1 and Therapymentioning

confidence: 99%

“…Similarly, MALAT1 promoted CPC proliferation and migration under hypoxic conditions via sponging miR‐125. Jumonji domain‐containing protein 6 (JMJD6) was a target of miR‐125 and JMJD6 knockdown blocked miR‐125 inhibitor's protective effect on CPC function in hypoxia …”

Section: Malat1 and Therapymentioning

confidence: 99%

“…15 MALAT1 was upregulated by hypoxia and could promote the proliferation and migration potential of cardiac stem cells (CSCs) and cardiac progenitor cells (CPCs) via sponging miR-155 or miR-125, respectively. 13,16 However, inhibition of MALAT1 induced a characteristic phenotype switching from a proliferative toward a more migratory pattern loss in vascular smooth muscle cells (VSMCs) and lead to significant cell cycle arrest in the G2 phase. 17 In addition, MALAT1 was also found to promote the proliferation of cardiomyocytes or ECs by activating of phosphoinositide-3-kinase (PI3K)/Protein kinase B (PKB, also called Akt) signaling or p38 mitogen-activated protein kinase (MAPK) signaling pathway, respectively.…”

Section: Proliferation/migrationmentioning

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 Pathophysiology Of Cvdsmentioning

confidence: 99%

Section: Malat1 and Therapymentioning

confidence: 99%

Section: Malat1 and Therapymentioning

confidence: 99%

Section: Proliferation/migrationmentioning

confidence: 99%

See 2 more Smart Citations

The role of lncRNA MALAT1 in cardiovascular disease

Yan

Song

et al. 2019

IUBMB Life

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“…The hypoxia‐inducible factor (HIF) hydroxylases are the major regulators of the hypoxia response, probably in animals ranging from nematode worms to man . Hypoxia can upregulate metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1), a long non‐coding RNA associated with cancer progression and metastasis . JMJD6 can be positively regulated by MALAT1 through MALAT1/miR‐125/JMJD6 axis.…”

Section: The Enzymatic Activities Of Jmjd6mentioning

confidence: 99%

Jumonji domain‐containing protein 6 protein and its role in cancer

et al. 2020

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The jumonji domain‐containing protein 6 (JMJD6) is a Fe(II)‐ and 2‐oxoglutarate (2OG)‐dependent oxygenase that catalyses lysine hydroxylation and arginine demethylation of histone and non‐histone peptides. Recently, the intrinsic tyrosine kinase activity of JMJD6 has also been reported. The JMJD6 has been implicated in embryonic development, cellular proliferation and migration, self‐tolerance induction in the thymus, and adipocyte differentiation. Not surprisingly, abnormal expression of JMJD6 may contribute to the development of many diseases, such as neuropathic pain, foot‐and‐mouth disease, gestational diabetes mellitus, hepatitis C and various types of cancer. In the present review, we summarized the structure and functions of JMJD6, with particular emphasis on the role of JMJD6 in cancer progression.

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Exploring links between 2‐oxoglutarate‐dependent oxygenases and Alzheimer's disease

Liu

Xie

Wang

et al. 2022

Alzheimer's & Dementia

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Hypoxia, that is, an inadequate oxygen supply, is linked to neurodegeneration and patients with cardiovascular disease are prone to Alzheimer's disease (AD). 2‐Oxoglutarate and ferrous iron‐dependent oxygenases (2OGDD) play a key role in the regulation of oxygen homeostasis by acting as hypoxia sensors. 2OGDD also have roles in collagen biosynthesis, lipid metabolism, nucleic acid repair, and the regulation of transcription and translation. Many biological processes in which the >60 human 2OGDD are involved are altered in AD patient brains, raising the question as to whether 2OGDD are involved in the transition from normal aging to AD. Here we give an overview of human 2OGDD and critically discuss their potential roles in AD, highlighting possible relationships with synapse dysfunction/loss. 2OGDD may regulate neuronal/glial differentiation through enzyme activity‐dependent mechanisms and modulation of their activity has potential to protect against synapse loss. Work linking 2OGDD and AD is at an early stage, especially from a therapeutic perspective; we suggest integrated pathology and in vitro discovery research to explore their roles in AD is merited. We hope to help enable long‐term research on the roles of 2OGDD and, more generally, oxygen/hypoxia in AD. We also suggest shorter term empirically guided clinical studies concerning the exploration of 2OGDD/oxygen modulators to help maintain synaptic viability are of interest for AD treatment.

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LncRNA-MALAT1 promotes CPC proliferation and migration in hypoxia by up-regulation of JMJD6 via sponging miR-125

Cited by 27 publications

References 28 publications

The role of lncRNA MALAT1 in cardiovascular disease

The role of lncRNA MALAT1 in cardiovascular disease

Jumonji domain‐containing protein 6 protein and its role in cancer

Exploring links between 2‐oxoglutarate‐dependent oxygenases and Alzheimer's disease

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