2. Academic Validation
  3. Macrophage erythropoietin signaling promotes macrophage-myofibroblast transformation and fibroblast-myofibroblast differentiation

Macrophage erythropoietin signaling promotes macrophage-myofibroblast transformation and fibroblast-myofibroblast differentiation

  • Biochem Biophys Res Commun. 2024 Nov 19:734:150783. doi: 10.1016/j.bbrc.2024.150783.
Pengfei Wu 1,  Wen Zhang 2,  Huiting Guan 3,  Tianrong Jin 4,  Jialin Jia 5,  Bangwei Luo 5,  Guansong Wang 2,  Zhiren Zhang 6
Affiliations

Affiliations

  • 1 Department of Pulmonary and Critical Care Medicine, Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University (Army Medical University), Chongqing, China; Department of Respiratory and Critical Care Medicine, Sichuan Science City Hospital, Mianyang, Sichuan, China.
  • 2 Department of Pulmonary and Critical Care Medicine, Institute of Respiratory Diseases, Xinqiao Hospital, Third Military Medical University (Army Medical University), Chongqing, China.
  • 3 Shenzhen Bao'an Traditional Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen, 518104, China.
  • 4 Medical College of Chongqing University, Chongqing, China.
  • 5 Institute of Immunology, Third Military Medical University (Army Medical University), Chongqing, China.
  • 6 Institute of Immunology, Third Military Medical University (Army Medical University), Chongqing, China. Electronic address: zhangzhiren@tmmu.edu.cn.
PMID: 39383829 DOI: 10.1016/j.bbrc.2024.150783
Abstract

While myofibroblasts are the key cause of abnormal extracellular matrix accumulation, the origin of which has not yet been fully elucidated. Recently, it has been found that macrophage-myofibroblast transformation (MMT) defined by the expression of both macrophage markers (F4/80 or CD68) and myofibroblast markers (α-SMA) is one of its important sources. In the process of MMT, it is unclear whether epor is involved. In this study, when BMDM was induced by TGF-β1, the number of F4/80+α-SMA+ cells increased, the cells polarized toward M2, and the expression of TGF-β1 increased. After the activation of epor, the number of F4/80 +α-SMA + cells and the polarization level of M2 were further increased. At the same time, we found that the conditioned medium from MMT cells could induce the activation of 3T3 cells with increased the expression of α-SMA and col-1. In contrast, the number of F4/80+α-SMA + cells, the polarization of M2, and the expression of TGF-β1 decreased after epor was inhibited by siRNA. Our results demonstrate that the activation of epor in BMDMs could promote the transformation of macrophage-myofibroblast induced by TGF-β1.

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