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GOLM1 Promotes Pulmonary Fibrosis through Upregulation of NEAT1.
Wang, Yani; Hu, Danjing; Wan, Linyan; Yang, Shuhui; Liu, Song; Wang, Zixi; Li, Jie; Li, Jia; Zheng, Zhoude; Cheng, Chongsheng; Wang, Yanan; Wang, Hanghang; Tian, Xinlun; Chen, Wenhui; Li, Shanqing; Zhang, Ji; Zha, Xiaojun; Chen, Jingyu; Zhang, Hongbing; Xu, Kai-Feng.
Afiliación
  • Wang Y; Department of Pulmonary and Critical Care Medicine and.
  • Hu D; Department of Pulmonary and Critical Care Medicine and.
  • Wan L; State Key Laboratory of Common Mechanism Research for Major Diseases, Haihe Laboratory of Cell Ecosystem, Department of Physiology, Institutes of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
  • Yang S; State Key Laboratory of Common Mechanism Research for Major Diseases, Haihe Laboratory of Cell Ecosystem, Department of Physiology, Institutes of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
  • Liu S; Medical Science Center, State Key Laboratory of Complex, Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
  • Wang Z; Department of Biochemistry & Molecular Biology, School of Basic Medicine, Anhui Medical University, Hefei, China.
  • Li J; State Key Laboratory of Common Mechanism Research for Major Diseases, Haihe Laboratory of Cell Ecosystem, Department of Physiology, Institutes of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
  • Li J; Department of Pulmonary and Critical Care Medicine and.
  • Zheng Z; Department of Pulmonary and Critical Care Medicine and.
  • Cheng C; Department of Pulmonary and Critical Care Medicine and.
  • Wang Y; State Key Laboratory of Common Mechanism Research for Major Diseases, Haihe Laboratory of Cell Ecosystem, Department of Physiology, Institutes of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
  • Wang H; Department of Pulmonary and Critical Care Medicine and.
  • Tian X; Department of Pulmonary and Critical Care Medicine and.
  • Chen W; Department of Lung Transplantation, Centre for Lung Transplantation, Centre for Respiratory Diseases, China-Japan Friendship Hospital, Beijing, China.
  • Li S; Department of Thoracic Surgery, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China; and.
  • Zhang J; Lung Transplantation Center, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi, China.
  • Zha X; Department of Biochemistry & Molecular Biology, School of Basic Medicine, Anhui Medical University, Hefei, China.
  • Chen J; Lung Transplantation Center, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi, China.
  • Zhang H; State Key Laboratory of Common Mechanism Research for Major Diseases, Haihe Laboratory of Cell Ecosystem, Department of Physiology, Institutes of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
  • Xu KF; Department of Pulmonary and Critical Care Medicine and.
Am J Respir Cell Mol Biol ; 70(3): 178-192, 2024 Mar.
Article en En | MEDLINE | ID: mdl-38029327
Idiopathic pulmonary fibrosis (IPF) is a lethal progressive disease with elusive molecular mechanisms and limited therapeutic options. Aberrant activation of fibroblasts is a central hallmark of lung fibrosis. Here, we report that Golgi membrane protein 1 (GOLM1, also known as GP73 or GOLPH2) was increased in the lungs of patients with pulmonary fibrosis and mice with bleomycin (BLM)-induced pulmonary fibrosis. Loss of GOLM1 inhibited proliferation, differentiation, and extracellular matrix deposition of fibroblasts, whereas overexpression of GOLM1 exerted the opposite effects. Similarly, worsening pulmonary fibrosis after BLM treatment was observed in GOLM1-knock-in mice, whereas BLM-treated Golm1-knockout mice exhibited alleviated pulmonary fibrosis and collagen deposition. Furthermore, we identified long noncoding RNA NEAT1 downstream of GOLM1 as a potential mediator of pulmonary fibrosis through increased GOLM1 expression. Depletion of NEAT1 inhibited fibroblast proliferation and extracellular matrix production and reversed the profibrotic effects of GOLM1 overexpression. Additionally, we identified KLF4 as a downstream mediator of GOLM1 signaling to NEAT1. Our findings suggest that GOLM1 plays a pivotal role in promoting pulmonary fibrosis through the GOLM1-KLF4-NEAT1 signaling axis. Targeting GOLM1 and its downstream pathways may represent a novel therapeutic strategy for treating pulmonary fibrosis.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Fibrosis Pulmonar Idiopática Límite: Animals / Humans Idioma: En Revista: Am J Respir Cell Mol Biol Asunto de la revista: BIOLOGIA MOLECULAR Año: 2024 Tipo del documento: Article

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Fibrosis Pulmonar Idiopática Límite: Animals / Humans Idioma: En Revista: Am J Respir Cell Mol Biol Asunto de la revista: BIOLOGIA MOLECULAR Año: 2024 Tipo del documento: Article