Open AccessCD 11b + interstitial macrophages are required for ischemia‐induced lung angiogenesis
Author(s) -
Moldobaeva Aigul,
Zhong Qiong,
Eldridge Lindsey,
Wagner Elizabeth M.
Publication year - 2018
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.13721
Subject(s) - angiogenesis , medicine , neovascularization , ischemia , lung , macrophage , integrin alpha m , immunology , pathology , pulmonary artery , cancer research , biology , immune system , biochemistry , in vitro
The importance of myeloid cells in promoting neovascularization has been shown in a number of pathological settings in several organs. However, the specific role of macrophages in promoting systemic angiogenesis during pulmonary ischemia is not fully determined. Our past work suggested that cells of monocytic lineage contributed to systemic angiogenesis in the lung since clodronate‐induced depletion of all macrophages resulted in attenuated neovascularization. Our current goals were to define the population of macrophages important for systemic vessel growth into the lung after the onset of pulmonary ischemia in mice. Interstitial macrophages ( CD 64 + Mer TK + CD 11b + ) increased significantly as did the percent of CD 45 + Ly6G + neutrophils 1 day after the induction of left lung ischemia, despite the fact there was limited cell recruitment due to complete obstruction of the left pulmonary artery in this ischemia model. Since both interstitial macrophages and neutrophils express CD 11b, we used CD 11b + DTR mice and showed the critical role for these cells since CD 11b + depleted mice showed no systemic angiogenesis 7 days after the onset of ischemia when compared to control mice. Coculture of mouse aortic endothelial cells with macrophages showed increased proliferation relative to endothelial cells in culture without inflammatory cells, or pulmonary artery endothelial cells. We conclude that CD 11b + leukocytes, trapped within the lung at the onset of ischemia, contribute to growth factor release, and are critical for new blood vessel proliferation.