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Characterization of Human Monocyte Subsets by Whole Blood Flow Cytometry Analysis
Published on: October 17, 2018
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Cardiac (myo)fibroblasts modulate the migration of monocyte subsets
Kathleen Pappritz1,2,3, Konstantinos Savvatis4,5, Annika Koschel1,3
1Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Internal Medicine and Cardiology, Campus Virchow Klinikum, Berlin, Germany.
Scientific Reports
|April 5, 2018
Summary
Interferon-gamma (IFN-γ) reduces transforming growth factor-beta 1 (TGF-β1)-induced cardiac fibroblast to myofibroblast differentiation but increases monocyte attraction. This suggests complex roles for these factors in cardiac inflammation and remodeling.
Area of Science:
- Cardiovascular Biology
- Immunology
- Cell Biology
Background:
- Cardiac fibroblasts are key regulators of the extracellular matrix and emerging inflammatory modulators.
- Interferon-gamma (IFN-γ) is known to inhibit transforming growth factor-beta 1 (TGF-β1)-induced myofibroblast differentiation.
- The effect of IFN-γ on TGF-β1-induced monocyte attraction in cardiac fibroblasts remains to be fully elucidated.
Purpose of the Study:
- To investigate the in vitro effects of IFN-γ on TGF-β1-induced monocyte attraction by cardiac fibroblasts.
- To analyze how combined TGF-β1 and IFN-γ stimulation influences fibroblast differentiation and chemokine release.
Main Methods:
- Cardiac fibroblasts (C4 and primary mouse LV fibroblasts) were stimulated with TGF-β1, IFN-γ, or both.
- Myofibroblast differentiation markers (Collagen I, III, α-SMA, LOX-1, LOXL-2) were quantified.
- Chemokine (CCL2, CCL7, Cx3CL1) release was measured, and monocyte subset migration (Ly6Clow, Ly6Chigh) towards conditioned media was analyzed.
Main Results:
- IFN-γ decreased TGF-β1-induced myofibroblast differentiation markers.
- Combined TGF-β1 + IFN-γ stimulation increased the release of CCL2, CCL7, and Cx3CL1 compared to TGF-β1 alone.
- TGF-β1 and IFN-γ conditioned media differentially attracted Ly6Clow and Ly6Chigh monocytes, respectively, with combined treatment reducing the Ly6Clow/Ly6Chigh migration ratio.
Conclusions:
- IFN-γ counteracts TGF-β1-induced myofibroblast differentiation in cardiac fibroblasts.
- IFN-γ enhances TGF-β1-induced monocyte attraction, altering the Ly6Clow/Ly6Chigh monocyte migration balance.
- These findings highlight the complex interplay of cytokines in cardiac remodeling and inflammation.
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