Neural Plasticity / 2019 / Article / Tab 3 / Review Article
M2 Macrophages as a Potential Target for Antiatherosclerosis Treatment Table 3 Receptors as potential targets for M2 polarization.
Targets Way to affect the targets Experiment animals or cells Effect Compounds or medicine References SR-A + SR-A-/- mice Lack of SR-A promotes M1 polarization by activating NF-κ B and suppressing STAT6 signaling [102 –105 ] Notch1R - THP-1 cells treated with Notch1R siRNA Enhanced M2 macrophage activation and upregulated anti-inflammatory cytokine secretion DAPT [106 ] Fcγ R - ApoE-/- Fcγ RIIb-/- mice Upregulated Arg1 and lower iNOS expression than ApoE-/- mice [107 , 108 ] Nr1D1 + Rev-erba knockdown mice Macrophages obtained from Rev-erba knockdown mice present lower M2 while overexpression of Rev-erba increased the expression of M2 markers. Heme promoted M2 marker expression Heme [111 ] Sdc-1 + Sdc-1+/+ and Sdc-1−/− macrophages Contributed to the motility that specifically induced M2 macrophage populations [112 ] KCa3.1 - Human monocytes; ApoE−/− mice on a C57BL/6 background Reduced plaque rupture and luminal thrombus in carotid arteries, decrease expression of M1 markers, and enhance expression of M2 markers within atherosclerotic lesion TRAM-34 [114 ]
SR-A: class A scavenger receptor; SR-A-/- mice: SR-A-deficient mice; Notgh1R: Notch1 receptor; THP-1 cells: a human monocytic cell line; Fcγ R: Fcγ receptors; iNOS: inducible nitric oxide synthase; Nr1D1: Rev-erba; Sdc-1: Syndecan-1; KCa3.1: calcium-activated potassium channel; DAPT: N-[N-(3,5-difluorophenacetyl)-l-alanyl]-S-phenylglycine t-butyl ester, a γ -secretase inhibitor; Sdc-1+/+ : wild-type macrophages; Sdc-1−/− macrophages: Sdc-1-deficient macrophages.