M1 and M2 macrophage proteolytic and angiogenic profile analysis in atherosclerotic patients reveals a distinctive profile in type 2 diabetes
Open accessAbstract
This study aimed to investigate atherosclerotic mediators’ expression levels in M1 and M2 macrophages and to focus on the influence of diabetes on M1/M2 profiles. Macrophages from 36 atherosclerotic patients (19 diabetics and 17 non-diabetics) were cultured with interleukin-1β (IL-1β) or IL-4 to induce M1 or M2 phenotype, respectively. The atherosclerotic mediators’ expression was evaluated by quantitative reverse transcription-polymerase chain reaction (RT-PCR). The results showed that M1 and M2 macrophages differentially expressed mediators involved in proteolysis and angiogenesis processes. The proteolytic balance (matrix metalloproteinase-9 (MMP-9)/tissue inhibitor of metalloproteinase-1 (TIMP-1), MMP-9/plasminogen activator inhibitor-1 (PAI-1) and MMP-9/tissue factor pathway inhibitor-2 (TFPI-2) ratios) was higher in M1 versus M2, whereas M2 macrophages presented higher angiogenesis properties (increased vascular endothelial growth factor/TFPI-2 and tissue factor/TFPI-2 ratios). Moreover, M1 macrophages from diabetics displayed more important proangiogenic and proteolytic activities than non-diabetics. This study reveals that M1 and M2 macrophages could differentially modulate major atherosclerosis-related pathological processes. Moreover, M1 macrophages from diabetics display a deleterious phenotype that could explain the higher plaque vulnerability observed in these subjects.
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The proteolytic balance, a ratio of MMP-9 to TIMP-1, is higher in M1 macrophages.
“the proteolytic balance, a ratio of MMP-9 to TIMP-1, is known to be higher in M1 macrophages39,40.”
From Bioengineered liver crosslinked with nano-graphene oxide enables efficient liver regeneration via MMP suppression and immunomodulation (2023) · cites this paper as [40]
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Macrophage phenotype in response to ECM bioscaffolds
Huleihel, L., Dziki, J. L., Bartolacci, J. G., Rausch, T., Scarritt, M. E., Cramer, M. C., Vorobyov, T., LoPresti, S. T., Swineheart, I. T., White, L. J., et al. (2017) · Seminars in Immunology · doi:10.1016/j.smim.2017.04.004 · Cited by 169 · see citing works
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Modulation of inflammatory M1-macrophages phenotype by valvular interstitial cells
Tagzirt, M., Rosa, M., Corseaux, D., Vincent, F., Vincentelli, A., Daoudi, M., Jashari, R., Staels, B., Van Belle, E., Susen, S., et al. (2023) · The Journal of Thoracic and Cardiovascular Surgery · doi:10.1016/j.jtcvs.2022.08.027 · Cited by 6 · see citing works
Self-citation
- Authors
- Roma-Lavisse, C., Tagzirt, M., Zawadzki, C., Lorenzi, R., Vincentelli, A., Haulon, S., Juthier, F., Rauch, A., Corseaux, D., Staels, B., Jude, B., Van Belle, E., Susen, S., Chinetti-Gbaguidi, G., & Dupont, A.
- Affiliations
- INSERM U1011, Laboratoire de Recherche J&K, Institut Pasteur de Lille, Faculté de Médecine – Pôle recherche, University of Lille Nord de France, EGID, Lille, France
- Inserm (FR)
- Cardiovascular and Pulmonary and Haematology Departments, University Hospital, Lille, France
- ORCID
- Venue
- Diabetes and Vascular Disease Research
- Publisher
- SAGE Publications
- Published
- 2015-05-11
- Volume
- 12
- Issue
- 4
- Pages
- 279-289
- ISSN
- 1479-1641 (ISSN-L)
- 1752-8984
- OpenAlex
- W2170723946
- Cited by
- 50
- References
- 2
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 4 · 2023: 5 · 2022: 7 · 2021: 2 · 2020: 4 · 2019: 4 · 2018: 4 · 2017: 10 · 2016: 6 · 2015: 1
- FWCI
- 3.45
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes and Vascular Disease Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Bristol-Myers Squibb
- Sanofi
- Agence Nationale de la Recherche
- Institut National de la Santé et de la Recherche Médicale
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
- Keywords
- M1 macrophages, M2 macrophages, atherosclerosis, type 2 diabetes, macrophage polarization, proteolysis, angiogenesis, MMP-9, TIMP-1, plasminogen activator inhibitor-1, TFPI-2, vascular endothelial growth factor, tissue factor, plaque vulnerability
- MeSH terms
- Mannose Receptor, Aged, Antigens, Surface, Carotid Artery Diseases, Cerebral Angiography, Coronary Artery Disease, Diabetes Mellitus, Type 2, Factor XIII, Female, Gene Expression Regulation, Glycoproteins, Humans, Macrophages, Male, Middle Aged, Neovascularization, Pathologic, Phenotype, Prospective Studies, Receptors, Cell Surface, Tumor Necrosis Factor-alpha, Cell Adhesion Molecules, Neuronal, Case-Control Studies, Receptors, Lymphocyte Homing, Interleukin-10, Coronary Angiography, Plasminogen Activator Inhibitor 1, Tissue Inhibitor of Metalloproteinase-1, Reverse Transcriptase Polymerase Chain Reaction, Matrix Metalloproteinase 9, Lectins, C-Type, Mannose-Binding Lectins, Atherosclerosis, Interleukin-1beta, Proteolysis, Orexin Receptors
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