HDAC inhibition helps post-MI healing by modulating macrophage polarization

Kimbrough, Denise; Wang, Sabina H.; Wright, Lillianne H.; Mani, Santhosh K.; Kasiganesan, Harinath; LaRue, Amanda C.; Cheng, Qi; Nadig, Satish N.; Atkinson, Carl; Menick, Donald R.

doi:10.1016/j.yjmcc.2018.04.011

Cited by 51 publications

(32 citation statements)

References 45 publications

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“…To correlate our in vitro analysis in BMDCs, showing that IGF1 induced CD206 + M2-like macrophage polarization, we used CD206 as a marker to identify reparative macrophages. 17 As shown in Figure 6B, treatment did not significantly affect the number of leukocytes (CD45 + ), neutrophils (CD11b + Ly6G + ), and macrophages (CD11b + Ly6G À F4/80 hi CD64 + ). However, analysis of macrophage subtypes showed that IGF1 substantially increased the mean number of CD206 + macrophages (152,777 ± 13,510 versus 108,071 ± 14,023, p = 0.041) without affecting the number of CD206 À macrophages.…”

Section: Igf1 Treatment Increases Cd206 + Macrophages In Cardiac Tissmentioning

confidence: 74%

IGF1 Treatment Improves Cardiac Remodeling after Infarction by Targeting Myeloid Cells

et al. 2019

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Section: Igf1 Treatment Increases Cd206 + Macrophages In Cardiac Tissmentioning

confidence: 74%

IGF1 Treatment Improves Cardiac Remodeling after Infarction by Targeting Myeloid Cells

et al. 2019

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“…This study identifies LAIR1 as a promising therapeutic target in atherosclerosis and related disorders. Another study demonstrated the involvement of histone deacetylases (HDAC) in the early recruitment of reparative CD45+/CD11b+/CD206+ macrophages to the heart after myocardial infarction and its positive correlation with the ventricular function and remodeling [ 30 ]. A study by Cao et al demonstrates that in the histone deacetylase 9 knockout mice ( Hdac9 -/- ), macrophages are inclined towards M2 phenotypes and show decreased expression of the pro-inflammatory M1 markers [ 31 ].…”

Section: Macrophages As Perfect Cells For Reprogrammingmentioning

confidence: 99%

Macrophage Modification Strategies for Efficient Cell Therapy

Poltavets

Vishnyakova

Elchaninov

et al. 2020

Cells

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Macrophages, important cells of innate immunity, are known for their phagocytic activity, capability for antigen presentation, and flexible phenotypes. Macrophages are found in all tissues and therefore represent an attractive therapeutic target for the treatment of diseases of various etiology. Genetic programming of macrophages is an important issue of modern molecular and cellular medicine. The controllable activation of macrophages towards desirable phenotypes in vivo and in vitro will provide effective treatments for a number of inflammatory and proliferative diseases. This review is focused on the methods for specific alteration of gene expression in macrophages, including the controllable promotion of the desired M1 (pro-inflammatory) or M2 (anti-inflammatory) phenotypes in certain pathologies or model systems. Here we review the strategies of target selection, the methods of vector delivery, and the gene editing approaches used for modification of macrophages.

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“…However, it should be noted that gene expression and molecular marker distribution changes induced in cultured macrophages are indeed biased toward a “classical” or “alternative” activation state as described by M1 and M2 [also suggested to be replaced by terms denoting the polarization stimulus, e.g., M(IL4) and M(IFN-γ) (132)]. Although these may not coincide to the in vivo states, some markers and cytokines are still used to describe polarization and the paradigm has not been fully abandoned in the literature, including the characterization of cardiac pathology [e.g., (136, 137)]. Interestingly, macrophages can also mimic other cardiac cell types.…”

Section: Cardiac Subpopulations and The Contribution Of Innate Immunitymentioning

confidence: 99%

Three in a Box: Understanding Cardiomyocyte, Fibroblast, and Innate Immune Cell Interactions to Orchestrate Cardiac Repair Processes

Psarras

Beis

Nikouli

et al. 2019

Front. Cardiovasc. Med.

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Following an insult by both intrinsic and extrinsic pathways, complex cellular, and molecular interactions determine a successful recovery or inadequate repair of damaged tissue. The efficiency of this process is particularly important in the heart, an organ characterized by very limited regenerative and repair capacity in higher adult vertebrates. Cardiac insult is characteristically associated with fibrosis and heart failure, as a result of cardiomyocyte death, myocardial degeneration, and adverse remodeling. Recent evidence implies that resident non-cardiomyocytes, fibroblasts but also macrophages -pillars of the innate immunity- form part of the inflammatory response and decisively affect the repair process following a cardiac insult. Multiple studies in model organisms (mouse, zebrafish) of various developmental stages (adult and neonatal) combined with genetically engineered cell plasticity and differentiation intervention protocols -mainly targeting cardiac fibroblasts or progenitor cells-reveal particular roles of resident and recruited innate immune cells and their secretome in the coordination of cardiac repair. The interplay of innate immune cells with cardiac fibroblasts and cardiomyocytes is emerging as a crucial platform to help our understanding and, importantly, to allow the development of effective interventions sufficient to minimize cardiac damage and dysfunction after injury.

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HDAC inhibition helps post-MI healing by modulating macrophage polarization

Cited by 51 publications

References 45 publications

IGF1 Treatment Improves Cardiac Remodeling after Infarction by Targeting Myeloid Cells

IGF1 Treatment Improves Cardiac Remodeling after Infarction by Targeting Myeloid Cells

Macrophage Modification Strategies for Efficient Cell Therapy

Three in a Box: Understanding Cardiomyocyte, Fibroblast, and Innate Immune Cell Interactions to Orchestrate Cardiac Repair Processes

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