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Role of TLR2 in lung angiogenesis

After chronic left pulmonary artery ligation (LPAL) in mice, there is rapid neovascularization of the ischemic lung. We showed increased macrophage‐derived growth factors and a positive correlation between the number of lavaged macrophages and the magnitude of angiogenesis. In the current study, we questioned whether macrophage subpopulations with specific surface markers contributed differentially to angiogenesis. Using flow cytometry, we showed an increase in total macrophages based on forward/side scatter characteristics over the first 48 hrs in left lung homogenates after LPAL (n=4). Specifically, we saw a 70% increase in the number of Cd11b+/CD11c‐ macrophages 48 hrs after LPAL. With no inflow to the lung early after LPAL, changes in cell numbers represent proliferation and/or differentiation. Within this same cell population, toll‐like receptor 2 (TLR‐2) expression ranged from 80‐90%. To confirm that TLR‐2 plays a role in angiogenesis, we measured neovascularization 14 days after LPAL in TLR‐2 deficient mice. Angiogenic outcome (microspheres) decreased by 48% of the wild type response (n=4). These data suggest that TLR‐2 plays a role in macrophage activation, important for angiogenesis.