Mesenchymal stem cell-derived conditioned medium attenuate angiotensin II-induced aortic aneurysm growth by modulating macrophage polarization

J Cell Mol Med. 2019 Dec;23(12):8233-8245. doi: 10.1111/jcmm.14694. Epub 2019 Oct 4.

Abstract

Mesenchymal stem cells (MSCs) exhibit therapeutic benefits on aortic aneurysm (AA); however, the molecular mechanisms are not fully understood. The current study aimed to investigate the therapeutic effects and potential mechanisms of murine bone marrow MSC (BM-MSCs)-derived conditioned medium (MSCs-CM) on angiotensin II (AngII)-induced AA in apolipoprotein E-deficient (apoE-/- ) mice. Murine BM-MSCs, MSCs-CM or control medium were intravenously administrated into AngII-induced AA in apoE-/- mice. Mice were sacrificed at 2 weeks after injection. BM-MSCs and MSCs-CM significantly attenuated matrix metalloproteinase (MMP)-2 and MMP-9 expression, aortic elastin degradation and AA growth at the site of AA. These treatments with BM-MSCs and MSCs-CM also decreased Ly6chigh monocytes in peripheral blood on day 7 and M1 macrophage infiltration in AA tissues on day 14, whereas they increased M2 macrophages. In addition, BM-MSCs and MSCs-CM reduced MCP-1, IL-1Ra and IL-6 expression and increased IL-10 expression in AA tissues. In vitro, peritoneal macrophages were co-cultured with BM-MSCs or fibroblasts as control in a transwell system. The mRNA and protein expression of M2 macrophage markers were evaluated. IL-6 and IL-1β were reduced, while IL-10 was increased in the BM-MSC systems. The mRNA and protein expression of M2 markers were up-regulated in the BM-MSC systems. Furthermore, high concentration of IGF1, VEGF and TGF-β1 was detected in MSCs-CM. Our results suggest that MSCs-CM could prevent AA growth potentially through regulating macrophage polarization. These results may provide a new insight into the mechanisms of BM-MSCs in the therapy of AA.

Keywords: aortic aneurysm; conditioned medium; macrophage polarization; matrix metalloproteinases; mesenchymal stem cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiotensin II
  • Animals
  • Aorta / drug effects
  • Aorta / metabolism
  • Aorta / pathology
  • Aortic Aneurysm / chemically induced
  • Aortic Aneurysm / metabolism
  • Aortic Aneurysm / prevention & control*
  • Apolipoproteins E / deficiency
  • Apolipoproteins E / genetics
  • Bone Marrow Cells / metabolism*
  • Cells, Cultured
  • Coculture Techniques
  • Culture Media, Conditioned / pharmacology*
  • Gene Expression / drug effects
  • Interleukin-10 / genetics
  • Interleukin-10 / metabolism
  • Interleukin-6 / genetics
  • Interleukin-6 / metabolism
  • Macrophage Activation / drug effects*
  • Macrophage Activation / genetics
  • Macrophages / cytology
  • Macrophages / drug effects*
  • Macrophages / metabolism
  • Male
  • Matrix Metalloproteinase 2 / genetics
  • Matrix Metalloproteinase 2 / metabolism
  • Matrix Metalloproteinase 9 / genetics
  • Matrix Metalloproteinase 9 / metabolism
  • Mesenchymal Stem Cells / metabolism*
  • Mice, Knockout

Substances

  • Apolipoproteins E
  • Culture Media, Conditioned
  • Interleukin-6
  • Angiotensin II
  • Interleukin-10
  • Matrix Metalloproteinase 2
  • Matrix Metalloproteinase 9