Macrophages modulate the viability and growth of human mesenchymal stem cells
Abstract
Following myocardial infarction, tissue repair is mediated by the recruitment of monocytes and their subsequent differentiation into macrophages. Recent findings have revealed the dynamic changes in the presence of polarized macrophages with pro‐inflammatory (M1) and anti‐inflammatory (M2) properties during the early (acute) and late (chronic) stages of cardiac ischemia. Mesenchymal stem cells (MSCs) delivered into the injured myocardium as reparative cells are subjected to the effects of polarized macrophages and the inflammatory milieu. The present study investigated how cytokines and polarized macrophages associated with pro‐inflammatory (M1) and anti‐inflammatory (M2) responses affect the survival of MSCs. Human MSCs were studied using an in vitro platform with individual and combined M1 and M2 cytokines: IL‐1β, IL‐6, TNF‐α, and IFN‐γ (for M1), and IL‐10, TGF‐β1, TGF‐β3, and VEGF (for M2). In addition, polarization molecules (M1: LPS and IFN‐γ; M2: IL‐4 and IL‐13) and common chemokines (SDF‐1 and MCP‐1) found during inflammation were also studied. Indirect and direct co‐cultures were conducted using M1 and M2 polarized human THP‐1 monocytes. M2 macrophages and their associated cytokines supported the growth of hMSCs, while M1 macrophages and their associated cytokines inhibited the growth of hMSCs in vitro under certain conditions. These data imply that an anti‐inflammatory (M2) environment is more accommodating to the therapeutic hMSCs than a pro‐inflammatory (M1) environment at specific concentrations. J. Cell. Biochem. 114: 220–229, 2012. © 2012 Wiley Periodicals, Inc.
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Macrophages mediate MSC viability and proliferation in vitro.
“It has also been shown that macrophages mediate MSC viability and proliferation in vitro [79]”
From Biomaterial based modulation of macrophage polarization: a review and suggested design principles (2015) · cites this paper as [79]
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- Authors
- Freytes, D. O., Kang, J. W., Marcos‐Campos, I., & Vunjak‐Novakovic, G.
- Affiliations
- Columbia University (US)
- Venue
- Journal of Cellular Biochemistry
- Publisher
- Wiley
- Published
- 2012-11-14
- Volume
- 114
- Issue
- 1
- Pages
- 220-229
- ISSN
- 0730-2312 (ISSN-L)
- 1097-4644
- OpenAlex
- W2095029191
- Cited by
- 255
- References
- 31
- Citations by year
- 2026: 5 · 2025: 13 · 2024: 14 · 2023: 12 · 2022: 29 · 2021: 21 · 2020: 19 · 2019: 21 · 2018: 22 · 2017: 27 · 2016: 15 · 2015: 20 · 2014: 20 · 2013: 11 · 2012: 4
- FWCI
- 8.38
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Cellular Biochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (2r01hl076485-16)
- National Heart, Lung, and Blood Institute (HL108668, R21HL108668, R01-HL076485, HL076485)
- National Institute of Biomedical Imaging and Bioengineering (EB-002520, P41EB002520)
- Topics
- Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- mesenchymal stem cells, macrophage polarization, M1 macrophages, M2 macrophages, myocardial infarction, cardiac regeneration, cytokines, IL-10, TGF-β1, vascular endothelial growth factor, chemokines, CXCL12, MCP-1, THP-1 cells, cell viability, cell growth, inflammation
- MeSH terms
- Cell Communication, Cell Line, Cell Survival, Humans, Inflammation, Lipopolysaccharides, Macrophages, Models, Biological, Cytokines, Coculture Techniques, Vascular Endothelial Growth Factor A, Cell Proliferation, Mesenchymal Stem Cells
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