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TGF-β1 suppresses CCL3/4 expression through the ERK signaling pathway and inhibits intervertebral disc degeneration and inflammation-related pain in a rat model.TGF-β1 通过 ERK 信号通路抑制 CCL3/4 的表达,从而抑制大鼠模型中椎间盘退变和炎症相关疼痛。
Exp Mol Med. 2017 Sep 22;49(9):e379. doi: 10.1038/emm.2017.136.
2
Syndecan-2 cytoplasmic domain up-regulates matrix metalloproteinase-7 expression via the protein kinase Cγ-mediated FAK/ERK signaling pathway in colon cancer.Syndecan-2胞质结构域通过蛋白激酶Cγ介导的FAK/ERK信号通路上调结肠癌中基质金属蛋白酶-7的表达。
J Biol Chem. 2017 Sep 29;292(39):16321-16332. doi: 10.1074/jbc.M117.793752. Epub 2017 Aug 16.
3
Osteoblastic heparan sulfate glycosaminoglycans control bone remodeling by regulating Wnt signaling and the crosstalk between bone surface and marrow cells.成骨细胞硫酸乙酰肝素糖胺聚糖通过调节Wnt信号以及骨表面与骨髓细胞之间的相互作用来控制骨重塑。
Cell Death Dis. 2017 Jun 29;8(6):e2902. doi: 10.1038/cddis.2017.287.
4
Transforming Growth Factor-β Modulates the Expression of Syndecan-4 in Cultured Vascular Endothelial Cells in a Biphasic Manner.转化生长因子-β以双相方式调节培养的血管内皮细胞中Syndecan-4的表达。
J Cell Biochem. 2017 Aug;118(8):2009-2017. doi: 10.1002/jcb.25861. Epub 2017 Apr 10.
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Non-specific low back pain.非特异性下背痛。
Lancet. 2017 Feb 18;389(10070):736-747. doi: 10.1016/S0140-6736(16)30970-9. Epub 2016 Oct 11.
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Cannabinoid WIN‑55,212‑2 mesylate inhibits ADAMTS‑4 activity in human osteoarthritic articular chondrocytes by inhibiting expression of syndecan‑1.大麻素WIN-55,212-2甲磺酸盐通过抑制syndecan-1的表达来抑制人骨关节炎关节软骨细胞中的ADAMTS-4活性。
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7
Syndecan-4 in intervertebral disc and cartilage: Saint or synner?椎间盘和软骨中的Syndecan-4:是圣徒还是同谋?
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8
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Blocking the function of inflammatory cytokines and mediators by using IL-10 and TGF-β: a potential biological immunotherapy for intervertebral disc degeneration in a beagle model.利用白细胞介素-10和转化生长因子-β阻断炎性细胞因子和介质的功能:比格犬模型中椎间盘退变的一种潜在生物免疫疗法。
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转化生长因子-β1通过细胞外调节蛋白激酶信号通路抑制髓核细胞中syndecan-2的表达。

TGF-β1 suppresses syndecan-2 expression through the ERK signaling pathway in nucleus pulposus cells.

作者信息

Yan Weifeng, Wang Xiaolin, Pei Yuxin, Chen Fan, Wang Jianru

机构信息

Department of Orthopaedics, The Hospital of Zhejiang General Corps of Armed Police Forces Jiaxing, China.

Guangdong Institute of Gastroenterology, Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, The 6th Affiliated Hospital of Sun Yat-sen University Guangzhou, China.

出版信息

Int J Clin Exp Pathol. 2018 Apr 1;11(4):2017-2024. eCollection 2018.

PMID:31938308
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6958228/
Abstract

Intervertebral disc degeneration (IVDD) is the main cause of low back pain and has become a worldwide problem causing enormous economic loss. Thus, mechanisms and treatment of IVDD are attracting great attention from surgeons and physicians. The syndecan (SDC) family has been reported to play important roles in various physiopathologic processes. In this study, we found that SDC2 expression levels were positively correlated with IVDD grades in human samples. Moreover, we demonstrated that transforming growth factor-β1 inhibited SDC2 expression through ERK1/2 signaling pathway activation in nucleus pulposus cells. Knocking down SDC2 in disc cells significantly suppressed aggrecanase-1 and aggrecanase-2 expression. The results of our study indicate that SDC2 may be a therapeutic target through which extracellular matrix degradation of IVDD can be controlled.

摘要

椎间盘退变(IVDD)是腰痛的主要原因,已成为一个导致巨大经济损失的全球性问题。因此,IVDD的发病机制及治疗方法正引起外科医生和内科医生的高度关注。据报道,多功能蛋白聚糖(SDC)家族在多种生理病理过程中发挥重要作用。在本研究中,我们发现人样本中SDC2的表达水平与IVDD分级呈正相关。此外,我们证明转化生长因子-β1通过激活髓核细胞中的ERK1/2信号通路来抑制SDC2表达。敲低椎间盘细胞中的SDC2可显著抑制聚集蛋白聚糖酶-1和聚集蛋白聚糖酶-2的表达。我们的研究结果表明,SDC2可能是一个治疗靶点,通过该靶点可以控制IVDD的细胞外基质降解。