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Macrophage microRNA-155 promotes cardiac hypertrophy and failure
Stephane Heymans1, Maarten F Corsten, Wouter Verhesen
1Center for Heart Failure Research, Department of Cardiology (S.H., M.F.C., W.V., P.C., R.E.W.v.L., K.C., T.P., M.H., M.v.B., A.-P.P., B.S.), Department of Molecular Genetics (L.S., M.P.J.d.W.), Department of Pathology (E.W., E.L.), Department of Pharmacology (B.J.J.), Department of Cardiology (L.J.d.W.), and Department of Internal Medicine (K.W.), Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, the Netherlands; Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands (S.H.); Center for Molecular and Cardiovascular Biology, Department of Cardiovascular Sciences, Leuven, Belgium (S.H., P.C., A.-P.P.); Department of Medical Biochemistry (L.S., E.L., M.P.J.d.W.) and Heart Failure Research Center (E.E.C., Y.M.P.), Academic Medical Center, Amsterdam, the Netherlands; Cluster of Excellence Cell Networks, Department of Infectious Diseases/Virology, Virus Host Interactions, Heidelberg University, Heidelberg, Germany (D.G., N.S.); Laboratory of Lymphocyte Signaling and Development, Babraham Institute, Cambridge, UK (E.V.); Institute for Molecular and Translational Therapeutic Strategies, Hannover Medical School, Hannover, Germany (T.T.); Medical Microbiology, Maastricht University, Maastricht, the Netherlands (F.S.); King's BHF Centre, King's College London, London UK (X.Y., M.M.); Institute for Cardiovascular Prevention, Ludwig Maximilians University, Munich, Germany (E.L.); and Molecular Medicine Laboratory, International Centre for Genetic Engineering and Biotechnology, Trieste, Italy (S.Z., M.G.).
MicroRNA-155 in macrophages drives cardiac inflammation and hypertrophy in hypertension. Inhibiting microRNA-155 in macrophages offers a potential therapy for hypertensive heart disease and failure.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Immunology
Background:
- Hypertension-induced cardiac hypertrophy and heart failure are significant research challenges.
- Inflammatory signaling pathways are increasingly recognized as therapeutic targets.
- MicroRNA-155 was previously identified as a key mediator of cardiac inflammation in infectious myocarditis.
Purpose of the Study:
- To investigate the role of microRNA-155 in the context of hypertensive heart disease.
- To determine the impact of manipulating microRNA-155 on cardiac inflammation, hypertrophy, and dysfunction under pressure overload.
Main Methods:
- Utilized genetic knockout and pharmacological inhibition of microRNA-155 in mice.
- Employed cardiomyocyte-specific microRNA-155 manipulation.
- Performed bone marrow transplantation experiments to assess macrophage dependence.
- Conducted in vitro studies using macrophage-conditioned media and cardiomyocyte co-cultures.
- Investigated the role of suppressor of cytokine signaling 1 (Socs1) as a microRNA-155 target.
Main Results:
- Loss or inhibition of microRNA-155 in leukocytes significantly reduced cardiac inflammation, hypertrophy, and dysfunction in pressure-overloaded mice.
- The effects were macrophage-dependent, as cardiomyocyte-specific manipulation had no impact, and bone marrow transplantation modulated the hypertrophic response.
- Macrophage-derived microRNA-155 influenced cardiomyocyte growth in a paracrine manner.
- Suppressor of cytokine signaling 1 (Socs1) was identified as a key mediator, with its knockdown partially restoring the hypertrophy-stimulating capacity of microRNA-155 deficient macrophages.
Conclusions:
- MicroRNA-155 expression in macrophages is a critical driver of cardiac inflammation, hypertrophy, and failure in response to pressure overload.
- These findings highlight the causative role of inflammatory signaling in hypertrophic heart disease.
- Targeting microRNA-155 in macrophages presents a feasible therapeutic strategy for heart failure associated with hypertension.
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