[HTML][HTML] CD36, but not G2A, modulates efferocytosis, inflammation, and fibrosis following bleomycin-induced lung injury [S]
BW Parks, LL Black, KA Zimmerman, AE Metz… - Journal of lipid …, 2013 - ASBMB
Macrophage G2A and CD36 lipid receptors are thought to mediate efferocytosis following
tissue injury and thereby prevent excessive inflammation that could compromise tissue
repair. To test this, we subjected mice lacking G2A or CD36 receptor to bleomycin-induced
lung injury and measured efferocytosis, inflammation, and fibrosis. Loss of CD36 (but not
G2A) delayed clearance of apoptotic alveolar cells (mean 78% increase in apoptotic cells 7
days postinjury), potentiated inflammation (mean 56% increase in lung neutrophils and 75 …
tissue injury and thereby prevent excessive inflammation that could compromise tissue
repair. To test this, we subjected mice lacking G2A or CD36 receptor to bleomycin-induced
lung injury and measured efferocytosis, inflammation, and fibrosis. Loss of CD36 (but not
G2A) delayed clearance of apoptotic alveolar cells (mean 78% increase in apoptotic cells 7
days postinjury), potentiated inflammation (mean 56% increase in lung neutrophils and 75 …