Interaction of macrophages with apoptotic cells inhibits transdifferentiation and invasion of lung fibroblasts

Yong Bae Kim, Young So Yoon, Youn Hee Choi, Eun Mi Park, Jihee Lee Kang

Research output: Contribution to journalArticlepeer-review

4 Scopus citations


The invasion of activated fibroblasts is a key mechanism of tissue fibrosis pathology. The recognition and uptake of apoptotic cells can induce the antifibrogenic programming of macrophages. We demonstrate that after interacting with apoptotic cells, macrophages secrete bioactive molecules that antagonize TGF-β1-induced increases in myofibroblast (fibroproliferative) phenotypic markers and reduce the enhanced invasive capacity of TGF-β1- or EGF-treated mouse lung fibroblasts (MLg). Furthermore, numerous treatment strategies prevented the anti-fibrotic effects of conditioned media, including transfection of macrophages with COX-2 or RhoA siRNAs or treatment of MLg cells with receptor antagonists for prostaglandin E2 (PGE2), PGD2, or hepatocyte growth factor (HGF). Additionally, administration of apoptotic cells in vivo inhibited the bleomycin-mediated invasive capacity of primary fibroblasts, as well as adhesion and extracellular matrix protein mRNA expression. These data suggest that the anti-fibrogenic programming of macrophages by apoptotic cells can be used as a novel tool to control the progressive fibrotic reaction.

Original languageEnglish
Pages (from-to)112297-112312
Number of pages16
Issue number68
StatePublished - 2017

Bibliographical note

Publisher Copyright:
© Kim et al.


  • Apoptotic cells
  • Invasion
  • Lung fibroblasts
  • Macrophages
  • Myofibroblast


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