title: Crosstalk of mesenchymal stem cells and macrophages promotes cardiac muscle repair.
abstract: Transplantation of bone-marrow derived mesenchymal stem cells (MSCs) has potential therapeutic effects on cardiac muscle repair. However, the underlying mechanism remains not completely clarified. Here we show that transplantation of MSCs significantly increased local recruitment of macrophages to facilitate cardiac muscle repair. MSCs-induced recovery of cardiac function and attenuation of fibrosis after injury were all abolished by either impaired macrophage infiltration, or by MSCs depletion after macrophage recruitment. However, angiogenesis seemed to be only affected by depletion of macrophages, but not by depletion of MSCs, suggesting that macrophages are responsible for the augmented angiogenesis after MSCs transplantation, while MSCs do not directly contribute to angiogenesis in the functional cardiac repair. Moreover, high level of transforming growth factor β 1 (TGFβ1) was detected in macrophages and high level of BMP7 was detected in MSCs, suggesting that MSCs not only may recruit macrophages to enhance angiogenesis to promote regeneration, but also may secrete BMP7 to contradict the fibrogenic effect of TGFβ1 by macrophages. Our study thus sheds new insight on the interaction of MSCs and macrophages in a functional cardiac repair triggered by MSCs transplantation.
authors.affiliation: Department of Cardiology, the Second Hospital of Hebei Medical University, 215 Hepingxin Road, Shijiazhuang, China.
authors.forename: Mei
authors.initials: M
authors.lastname: Wang
authors.affiliation: Department of Cardiology, the Second Hospital of Hebei Medical University, 215 Hepingxin Road, Shijiazhuang, China.
authors.forename: Guoru
authors.initials: G
authors.lastname: Zhang
authors.affiliation: Department of Cardiology, the Second Hospital of Hebei Medical University, 215 Hepingxin Road, Shijiazhuang, China.
authors.forename: Yaling
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Cardiology, the Second Hospital of Hebei Medical University, 215 Hepingxin Road, Shijiazhuang, China.
authors.forename: Tao
authors.initials: T
authors.lastname: Liu
authors.affiliation: Department of Cardiology, the Second Hospital of Hebei Medical University, 215 Hepingxin Road, Shijiazhuang, China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Department of Cardiology, the Second Hospital of Hebei Medical University, 215 Hepingxin Road, Shijiazhuang, China.
authors.forename: Yu
authors.initials: Y
authors.lastname: An
authors.affiliation: Department of Cardiology, the Second Hospital of Hebei Medical University, 215 Hepingxin Road, Shijiazhuang, China. Electronic address: yongjun_li14@163.com.
authors.forename: Yongjun
authors.initials: Y
authors.lastname: Li
mesh_terms: D000818:Animals; D055419:Bone Morphogenetic Protein 7 / Q000235:genetics / Q000378:metabolism; D005434:Flow Cytometry; D007150:Immunohistochemistry; D008264:Macrophages / Q000166:cytology / Q000378:metabolism*; D008297:Male; D059630:Mesenchymal Stem Cells / Q000166:cytology / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D009206:Myocardium; D053773:Transforming Growth Factor beta1 / Q000378:metabolism
chemical_list: D055419:Bone Morphogenetic Protein 7; D053773:Transforming Growth Factor beta1; C525820:bmp7 protein, mouse
keywords: BMP7; Cardiac muscle repair; Macrophages; Mesenchymal stem cells; Transforming growth factor β 1