TET2 is involved in DNA hydroxymethylation, cell proliferation and inflammatory response in keratinocytes

Liu, Xinxin; Wang, Xin; Liu, Nian; Zhu, Ke; Zhang, Song; Duan, Xiaoru; Huang, Yongjun; Jin, Zhao-Hui; Jaypaul, Himanshu; Wu, Yan; Chen, Hong-Xiang

doi:10.3892/mmr.2020.10989

Cited by 12 publications

(7 citation statements)

References 36 publications

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“…Furthermore, the role of TET2 in regulating skin in ammatory and skin disorders has also been found. Recent studies showed that knockdown of TET2 greatly improved HaCaT cell viability, lessened the psoriasiform phenotype and reduced the level of proin ammatory cytokines in mice (28,31). In this work, we noticed that deletion of TET2 effectively prevented photodamage caused by UVB in vitro and vivo.…”

Section: Discussionmentioning

confidence: 51%

TET2 amplifies RIPK3/MLKL necroptosis signal by upregulation of PLK3 to promote UVB-induced skin photodamage

Wang

Yang

Zeng

et al. 2023

Preprint

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The ultraviolet B (UVB) radiation causes cell death, reactive oxygen species (ROS) accumulation and skin inflammation, which leads to skin photodamage, including skin photoaging, photodermatoses, pigmentary disorders or even skin cancers. However, the mechanism of UVB-induced skin damage remains poorly understood. Here, we find that the expression of ten-eleven translocation 2 (TET2) is upregulated in UVB-irradiated cells and skin tissue. This upregulation leads to increased accumulation of reactive oxygen species (ROS) and cell death, as well as the release of matrix metalloproteinase-1 (MMP-1) and interleukin 6 (IL-6), which accelerates necroinflammation in UVB-irradiated mouse skin. Moreover, the study found that TET2 promotes skin photodamage induced by UVB by upregulating the protein kinase 3 (RIPK3)-mixed lineage kinase domain-like (MLKL) related necroptosis. Mechanistically, TET2 interacts with RIPK3 and MLKL via upregulated polo-like kinase 3 (PLK3), which leads to increased activation of the RIPK3/MLKL/necroptosis signal. These findings have important implications for the prevention and treatment of skin diseases caused by UVB irradiation. By better understanding the mechanisms underlying UVB-induced skin damage, researchers and clinicians may be better equipped to develop strategies for protecting against or treating these conditions.

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Section: Discussionmentioning

confidence: 51%

TET2 amplifies RIPK3/MLKL necroptosis signal by upregulation of PLK3 to promote UVB-induced skin photodamage

Wang

Yang

Zeng

et al. 2023

Preprint

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“…The optical density (OD) values were measured at 490 nm, and the OD of each group at each time point was recorded to plot the curve. C Proliferation-related markers were detected by Western blot of DNA 5-methylcytosine and is involved in cell apoptosis [33]. Previous studies showed that TET2 was downregulated during the pathogenesis of atherosclerosis [34].…”

Section: Discussionmentioning

confidence: 99%

Micro-RNA-338-3p Promotes the Development of Atherosclerosis by Targeting Desmin and Promoting Proliferation

Yan

Chen

Zhang³

et al. 2021

Mol Biotechnol

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Atherosclerosis (AS) is a dynamic and multi-stage process that involves various cells types, such as vascular smooth muscle cells (VSMCs) and molecules such as microRNAs. In this study, we investigated how miR-338-3p works in the process of AS. To determine how miR-338-3p was expressed in AS, an AS rat model was established and primary rat VSMCs were cultured. Real-time polymerase chain reaction was performed to detect miR-338-3p expression. Markers of different VSMC phenotypes were tested by Western blot. Immunofluorescent staining was employed to observe the morphologic changes of VSMCs transfected with miR-338-3p mimics. A dual luciferase reporter assay system was used to verify that desmin was a target of miR-338-3p. To further identify the role of miR-338-3p in the development of AS, VSMC proliferation and migration were evaluated by EdU incorporation assay, MTT assay, and wound healing assay. miR-338-3p expression was upregulated in the aortic tissues of an AS rat model and in primary rat VSMCs from a later passage. The transfection of miR-338-3p mimics in VSMCs promoted the synthetic cell phenotype. Bioinformatics analysis proposed desmin as a candidate target for miR-338-3p and the dual luciferase reporter assay confirmed in vivo that desmin was a direct target of miR-338-3p. The MTT and EdU incorporation assay revealed increased cell viability when miR-338-3p mimics were transfected. The increased expression of PCNA was a consistent observation, although a positive result was not obtained with respect to VSMC mobility. In AS, miR-338-3p expression was elevated. Elevated miR-338-3p inhibited the expression of desmin, thus promoting the contractile-to-synthetic VSMC phenotypic transition. In addition to morphologic changes, miR-338-3p enhanced the proliferative but not mobile ability of VSMCs. In summary, miR-338-3p promotes the development of AS.

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“…104 Liu and colleagues suggested that Tet2 can induce p16 expression and that knockdown of Tet2 decreases the level of p16 expression. 105 Sik1, an AMPK-related protein kinase, interacts with Sld5 in the GINS complex at sites of DNA replication during G1 phase at the onset of S phase. Sik1 phosphorylates MCM2 at its N-terminus to activate the MCM helicase, which is essential for the initiation of DNA replication.…”

Section: Regulation Of the Cell Cycle By Rhythmically Expressed Cell ...mentioning

confidence: 99%

The molecular circadian rhythms regulating the cell cycle

Zhou,

Wang,

et al. 2024

J of Cellular Biochemistry

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The circadian clock controls the expression of a large proportion of protein‐coding genes in mammals and can modulate a wide range of physiological processes. Recent studies have demonstrated that disruption or dysregulation of the circadian clock is involved in the development and progression of several diseases, including cancer. The cell cycle is considered to be the fundamental process related to cancer. Accumulating evidence suggests that the circadian clock can control the expression of a large number of genes related to the cell cycle. This article reviews the mechanism of cell cycle‐related genes whose chromatin regulatory elements are rhythmically occupied by core circadian clock transcription factors, while their RNAs are rhythmically expressed. This article further reviews the identified oscillatory cell cycle‐related genes in higher organisms such as baboons and humans. The potential functions of these identified genes in regulating cell cycle progression are also discussed. Understanding how the molecular clock controls the expression of cell cycle genes will be beneficial for combating and treating cancer.

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TET2 is involved in DNA hydroxymethylation, cell proliferation and inflammatory response in keratinocytes

Cited by 12 publications

References 36 publications

TET2 amplifies RIPK3/MLKL necroptosis signal by upregulation of PLK3 to promote UVB-induced skin photodamage

TET2 amplifies RIPK3/MLKL necroptosis signal by upregulation of PLK3 to promote UVB-induced skin photodamage

Micro-RNA-338-3p Promotes the Development of Atherosclerosis by Targeting Desmin and Promoting Proliferation

The molecular circadian rhythms regulating the cell cycle

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