2篇
您的检索式：作者名="Ruoxuan Yang"
|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | LncRNA DACH1 protects against pulmonary fibrosis by binding to SRSF1 to suppress CTNNB1 accumulation显示文摘Idiopathic pulmonary fibrosis(IPF)is a progressive disease with unknown etiology and limited therapeutic options.Activation of fibroblasts is a prominent feature of pulmonary fibrosis.Here we report that lncRNA DACH1(dachshund homolog 1)is downregulated in the lungs of IPF patients and in an experimental mouse model of lung fibrosis.LncDACH1 knockout mice develop spontaneous pulmonary fibrosis,whereas overexpression of LncDACH1 attenuated TGF-β1-induced aberrant activation,collagen deposition and differentiation of mouse lung fibroblasts.Similarly,forced expression of LncDACH1 not only prevented bleomycin(BLM)-induced lung fibrosis,but also reversed established lung fibrosis in a BLM model.Mechanistically,LncDACH1 binding to the serine/arginine-rich splicing factor 1(SRSF1)protein decreases its activity and inhibits the accumulation of Ctnnb1.Enhanced expression of SRSF1 blocked the anti-fibrotic effect of LncDACH1 in lung fibroblasts.Furthermore,loss of LncDACH1 promoted proliferation,differentiation,and extracellular matrix(ECM)deposition in mouse lung fibroblasts,whereas such effects were abolished by silencing of Ctnnb1.In addition,a conserved fragment of LncDACH1 alleviated hyperproliferation,ECM deposition and differentiation of MRC-5 cells driven by TGF-β1.Collectively,LncDACH1 inhibits lung fibrosis by interacting with SRSF1 to suppress CTNNB1 accumulation,suggesting that LncDACH1 might be a potential therapeutic target for pulmonary fibrosis. | Jian Sun Tongzhu Jin Zhihui Niu Jiayu Guo Yingying Guo Ruoxuan Yang Qianqian Wang Huiying Gao Yuhan Zhang Tianyu Li Wenxin He Zhixin Li Wenchao Ma Wei Su Liangliang Li Xingxing Fan Hongli Shan Haihai Liang | 2022 | Acta Pharmaceutica Sinica B2022，12，9： | 1 |
| 2 | DLX5 promotes Col10a1 expression and chondrocyte hypertrophy and is involved in osteoarthritis progression显示文摘Osteoarthritis(OA)has been considered non-reversible as articular cartilage wears down with limited repair capacity.Enhanced chondrocyte hypertrophy and increased type X collagen gene(COL10A1)expression have been associated with OA.Therefore,regulators controlling collagen X expression and chondrocyte hypertrophy may play a role in OA intervention.Here,we investigated how Distal-less homeobox 5(DLX5),the distal-less homeobox family member,controls murine Col10a1 gene expression and chondrocyte hypertrophy in chondrogenic cell models and its role in a murine OA model.Through qRT-PCR and Western blot analyses,we detected significantly increased levels of COL10A1 and DLX5 in hypertrophic MCT and ATDC5 cells compared to their proliferative stage.Forced expression of Dlx5 further increases,while knockdown of Dlx5 decreases COL10A1 expression in hypertrophic MCT cells.We have performed dual-luciferase reporter and ChiP assays and demonstrated that DLX5 promotes reporter activity through direct interaction with Col10a1 cis-enhancer.We established a murine OA model and detected markedly increased COL10A1 and DLX5 in the articular cartilage and subchondral bone of the OA mice compared with the controls.Notably,forced overexpression of DLX5 in hypertrophic MCT cells up-regulates RUNX2,and adjacent DLX5 and RUNX2 binding sites have previously been found within the Col10a1 cis-enhancer.Together,our data suggest that DLX5 may cooperate with RUNX2 to control cell-specific Col10a1 expression and chondrocyte hypertrophy and is involved in OA pathogenesis. | Jinnan Chen Fangzhou Chen Xuan Wu Huiqin Bian Chen Chen Xiaojing Zhang Ruoxuan Hei Xiaotong Yang Haochun Yuan Qian Wang Yaojuan Lu Longwei Qiao Qiping Zheng | 2023 | Genes & Diseases2023，10，5： | 1 |
您所在的机构暂未开通此部分的功能，请联系管理员