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Regulation of alternative macrophage activation by MSCs derived hypoxic conditioned medium, via the TGF-モ/Smad3 pathway
Ran Kim1 (Graduate Student), Byeong-Wook Song2 (Professor), Minji Kim1 (Graduate Student), Won Jung Kim1 (Graduate Student), Hee Won Lee1 (Graduate Student), Min Young Lee3 (Professor), Jongmin Kim4 (Professor), Woochul Chang 1,* (Professor)
1Department of Biology Education, Pusan National University,
2Department of Medical Science, Catholic Kwandong University,
3Department of Molecular Physiology, Kyungpook National University,
4Department of Life Systems, Sookmyung Women’s University
Macrophages are re-educated and polarized in response to myocardial infarction (MI). The M2 anti-inflammatory phenotype is a known dominator of late stage MI. Mesenchymal stem cells (MSCs) represent a promising tool for cell therapy, particularly heart related diseases. In general, MSCs induce alteration of the macrophage subtype from M1 to M2, both in vitro and in vivo. We conjectured that hypoxic conditions can promote properties of MSCs, including cell proliferation, migration and secretome production. Hypoxia induces TGF-モ1 expression, and TGF-モ1 mediates macrophage polarization to M2 phenotype for anti-inflammation and angiogenesis in infarcted areas. We hypothesized that macrophages undergo advanced M2 polarization after exposure to MSCs in hypoxia. Treatment of MSCs derived hypoxic conditioned medium (hypo-CM) promoted M2 macrophage polarization and neovascularization through the TGF-モ1/Smad3 pathway. In addition, hypo-CM derived from MSCs improved restoration of ischemic heart, such as attenuating cell apoptosis and fibrosis, and ameliorating microvessel density. Based on our results, we propose a new therapeutic method for effective MI treatment using regulation of macrophage polarization.
Abstract, Accepted Manuscript(in press) [Submitted on August 26, 2020, Accepted on October 5, 2020]
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