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Inhibition of Sirtuin 3 prevents titanium particle-induced bone resorption and osteoclastsogenesis via suppressing ERK and JNK signaling.抑制 Sirtuin 3 通过抑制 ERK 和 JNK 信号通路预防钛颗粒诱导的骨吸收和破骨细胞生成。
Int J Biol Sci. 2021 Apr 3;17(5):1382-1394. doi: 10.7150/ijbs.53992. eCollection 2021.
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The Role of Autophagy in Osteoclast Differentiation and Bone Resorption Function.自噬在破骨细胞分化和骨吸收功能中的作用。
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Punicalagin ameliorates wear-particle-induced inflammatory bone destruction by bi-directional regulation of osteoblastic formation and osteoclastic resorption.石榴皮鞣花素通过双向调节成骨细胞形成和破骨细胞吸收来改善磨损颗粒诱导的炎性骨破坏。
Biomater Sci. 2020 Sep 21;8(18):5157-5171. doi: 10.1039/d0bm00718h. Epub 2020 Aug 25.
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eIF2α signaling regulates autophagy of osteoblasts and the development of osteoclasts in OVX mice.eIF2α 信号通路调控去卵巢小鼠成骨细胞自噬和破骨细胞分化。
Cell Death Dis. 2019 Dec 4;10(12):921. doi: 10.1038/s41419-019-2159-z.
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Beclin1 Modulates Bone Homeostasis by Regulating Osteoclast and Chondrocyte Differentiation.Beclin1 通过调节破骨细胞和软骨细胞分化来调节骨稳态。
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Autophagy. 2019 Dec;15(12):2063-2075. doi: 10.1080/15548627.2019.1596491. Epub 2019 Apr 16.
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TET2 coactivates gene expression through demethylation of enhancers.TET2 通过去甲基化增强子来激活基因表达。
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Tet1 and Tet2 maintain mesenchymal stem cell homeostasis via demethylation of the P2rX7 promoter.Tet1 和 Tet2 通过 P2rX7 启动子的去甲基化维持间充质干细胞的内稳态。
Nat Commun. 2018 Jun 1;9(1):2143. doi: 10.1038/s41467-018-04464-6.

TET2 通过调节自噬来调节破骨细胞生成，从而调控去卵巢诱导的骨丢失。

TET2 regulates osteoclastogenesis by modulating autophagy in OVX-induced bone loss.

机构信息

Department of Orthopedics, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.

Department of Orthopedics, Zhangjiagang Tcm Hospital Affiliated to Nanjing University of Chinese Medicine, Zhangjiagang, Jiangsu, China.

出版信息

Autophagy. 2022 Dec;18(12):2817-2829. doi: 10.1080/15548627.2022.2048432. Epub 2022 Mar 24.

DOI:10.1080/15548627.2022.2048432
PMID:35255774
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9673923/
Abstract

Increased bone resorption by osteoclasts after estrogen deficiency is the main cause of postmenopausal osteoporosis. TET2 (tet methylcytosine dioxygenase 2) is a DNA demethylase that regulates cellular function and differentiation potential. Macroautophagy/autophagy maintains cellular homeostasis by recycling unnecessary and damaged organelles. This study revealed that TET2 promoted bone loss in oophorectomized (OVX) mice and that TET2 promoted osteoclast differentiation by regulating autophagy. knockdown inhibited autophagy and osteoclast differentiation in vitro. Mechanistically, knockdown increased BCL2 (B cell leukemia/lymphoma 2) expression and BCL2 exhibited increased binding to BECN1 and negatively regulated autophagy. Small interfering RNA specific to interfered with BCL2 expression in -knockdown bone marrow cells/precursors, partially reversing autophagy dysregulation and promoting osteoclast differentiation. Moreover, the LV-sh lentivirus prevented bone loss in OVX mice. In summary, our findings provide evidence that TET2 promotes osteoclast differentiation by inhibiting BCL2 expression and positively regulating BECN1-dependent autophagy.: ACP5/TRAP: acid phosphatase 5, tartrate resistant; ATP6V0D2: ATPase, H+ transporting, lysosomal V0 subunit D2; BCL2: B cell leukemia/lymphoma 2; BECN1: beclin 1, autophagy related; BMs: bone marrow cells; CTSK: cathepsin K; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MMP9: matrix metallopeptidase 9; OVX: oophorectomy; RUNX1: runt related transcription factor 1; SOCS3: suppressor of cytokine signaling 3; SPI1/PU.1: Spi-1 proto-oncogene; TNFSF11/RANKL: tumor necrosis factor (ligand) superfamily, member 11; TET2: tet methylcytosine dioxygenase 2.

摘要

破骨细胞中雌激素缺乏导致的骨吸收增加是绝经后骨质疏松症的主要原因。TET2（四甲基胞嘧啶双加氧酶 2）是一种调节细胞功能和分化潜能的 DNA 去甲基酶。巨自噬/自噬通过回收不必要和受损的细胞器来维持细胞内稳态。本研究揭示了 TET2 通过调节自噬促进去卵巢（OVX）小鼠的骨丢失，并且 TET2 通过调节自噬促进破骨细胞分化。抑制自噬和体外破骨细胞分化。在机制上，下调增加了 BCL2（B 细胞白血病/淋巴瘤 2）的表达，BCL2 与 BECN1 的结合增加，并负调控自噬。针对 的特异性小干扰 RNA（siRNA）干扰了 -敲低的骨髓细胞/前体细胞中的 BCL2 表达，部分逆转了自噬失调并促进了破骨细胞分化。此外，LV-sh 慢病毒防止了 OVX 小鼠的骨丢失。总之，我们的研究结果提供了证据，证明 TET2 通过抑制 BCL2 表达和正向调节 BECN1 依赖性自噬来促进破骨细胞分化。