Histone Demethylase Kdm2a Regulates Germ Cell Genes and Endogenous Retroviruses in Embryonic Stem Cells

Fu, Enze; Shen, Jian; Dong, Zhiqiang; Zhang, Weiyu; Zhang, Yongwang; Chen, Fuquan; Cheng, Zhi; Zhao, Xin; Shuai, Ling; Lu, Xinyi

doi:10.2217/epi-2018-0126

Cited by 11 publications

(5 citation statements)

References 54 publications

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“…KDM2A knockdown affects the expression of cell cycle regulatory factors, such as p21 Cip1 , which in turn decreases cell proliferation and increases apoptosis (64). KDM2A plays a vital role in maintaining embryonic stem cells by affecting the methylation levels of H3K36me2 and H3K4me3, and regulating the expression of germ cell-related genes (65). In the xenopus model, the stability of nuclear β-catenin depends on its methylation/demethylation, and the lysine demethylase Kdm2a/b specifically demethylates and degrades non-phosphorylated β-catenin in the nucleus to regulate the canonical Wnt signaling pathway, which plays a decisive role in the formation of the anterior-posterior body axis in xenopus embryos (66).…”

Section: Role Of Kdm2a In Cell Differentiation and Developmentmentioning

confidence: 99%

Histone demethylase KDM2A: Biological functions and clinical values (Review)

Liu

Lin

2021

Exp Ther Med

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Section: Role Of Kdm2a In Cell Differentiation and Developmentmentioning

confidence: 99%

Histone demethylase KDM2A: Biological functions and clinical values (Review)

Liu

Lin

2021

Exp Ther Med

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“…KDM2A, as a lysine (K)-specific histone demethylase, could selectively remove mono-and di-methylation from histone H3K36 and regulate H3K4me3. Several reports show that KDM2A influence cell proliferation, differentiation, senescence, apoptosis and tumorigenesis by exhibiting their H3K36 demethylase functions at specific genes sites [8,9]. KDM2A weakened osteo−/dentinogenic differentiation potential of MSCs via the combination with BCOR, then demethylating the histones in Epiregulin promoter to repress EREG transcription [10].…”

Section: Introductionmentioning

confidence: 99%

Depletion of SNRNP200 inhibits the osteo−/dentinogenic differentiation and cell proliferation potential of stem cells from the apical papilla

Yang

Shi

et al. 2020

BMC Dev Biol

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Background Tissue regeneration mediated by mesenchymal stem cells (MSCs) is deemed a desirable way to repair teeth and craniomaxillofacial tissue defects. Nevertheless, the molecular mechanisms about cell proliferation and committed differentiation of MSCs remain obscure. Previous researches have proved that lysine demethylase 2A (KDM2A) performed significant function in the regulation of MSC proliferation and differentiation. SNRNP200, as a co-binding factor of KDM2A, its potential effect in regulating MSCs’ function is still unclear. Therefore, stem cells from the apical papilla (SCAPs) were used to investigate the function of SNRNP200 in this research. Methods The alkaline phosphatase (ALP) activity assay, Alizarin Red staining, and osteogenesis-related gene expressions were used to examine osteo−/dentinogenic differentiation potential. Carboxyfluorescein diacetate, succinimidyl ester (CFSE) and cell cycle analysis were applied to detect the cell proliferation. Western blot analysis was used to evaluate the expressions of cell cycle-related proteins. Results Depletion of SNRNP200 caused an obvious decrease of ALP activity, mineralization formation and the expressions of osteo−/dentinogenic genes including RUNX2, DSPP, DMP1 and BSP. Meanwhile, CFSE and cell cycle assays revealed that knock-down of SNRNP200 inhibited the cell proliferation and blocked cell cycle at the G2/M and S phase in SCAPs. In addition, it was found that depletion of SNRNP200 up-regulated p21 and p53, and down-regulated the CDK1, CyclinB, CyclinE and CDK2. Conclusions Depletion of SNRNP200 repressed osteo−/dentinogenic differentiation potentials and restrained cell proliferation through blocking cell cycle progression at the G2/M and S phase, further revealing that SNRNP200 has crucial effects on preserving the proliferation and differentiation potentials of dental tissue-derived MSCs.

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“…Lysine demethylase 2A (KDM2A) is a demethylase, which plays an important role in transcriptional cell proliferation, angiogenesis, tumorigenesis regulation, and artificial induced pluripotent stem cell technology. [19][20][21][22] Bioinformatics software (TargetScan) predicts that KDM2A may be a target gene of miR-134-5p. Thus, we speculate that the role of miR-134-5p in MI may be related to KDM2A.…”

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confidence: 99%

MiR-134-5p Regulates Myocardial Apoptosis and Angiogenesis by Directly Targeting KDM2A After Myocardial Infarction

et al. 2020

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MiR-134-5p was found to have potential diagnostic value for myocardial infarction (MI), but its biological role in MI has not been reported. In this study, MI mouse model was established. Quantitative real-time PCR (qRT-PCR) and western blot were used to measure the expression of miR-134-5p, lysine demethylase 2A (KDM2A), and vascular endothelial growth factor (VEGF). Dual-Luciferase reporter (DLR) assay was used to explore the relationship between miR-134-5p and KDM2A. The influence of miR-134-5p on cardiomyocytes apoptosis was detected using methyl thiazolyl tetrazolium (MTT) assay. The results revealed that miR-134-5p was highly expressed in infarction tissues of MI mice. Knockdown of miR-134-5p inhibited hypoxia/reoxygenation (H/R)-induced cardiomyocyte apoptosis. In addition, KDM2A was the target gene of miR-134-5p and negatively regulated by miR-134-5p. The promotion effect on the protein level of KDM2A and VEGF induced by miR-134-5p inhibitor can be reversed by shKDM2A in cardiomyocytes. Further, silencing of miR-134-5p promoted myocardial angiogenesis and inhibited myocardial apoptosis via upregulating KDM2A in MI mice. Taken together, our research revealed that knockdown of miR-134-5p increased KDM2A expression, thereby suppressing myocardial apoptosis and promoting myocardial angiogenesis.

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Histone Demethylase Kdm2a Regulates Germ Cell Genes and Endogenous Retroviruses in Embryonic Stem Cells

Cited by 11 publications

References 54 publications

Histone demethylase KDM2A: Biological functions and clinical values (Review)

Histone demethylase KDM2A: Biological functions and clinical values (Review)

Depletion of SNRNP200 inhibits the osteo−/dentinogenic differentiation and cell proliferation potential of stem cells from the apical papilla

MiR-134-5p Regulates Myocardial Apoptosis and Angiogenesis by Directly Targeting KDM2A After Myocardial Infarction

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