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- W2108626579 abstract "Objective— The balance between apoptosis susceptibility and efferocytosis of macrophages is central to plaque remodeling and inflammation. LRP-1 and its ligand, apolipoprotein E, have been implicated in efferocytosis and apoptosis in some cell types. We investigated the involvement of the macrophage LRP-1/apolipoprotein E axis in controlling plaque apoptosis and efferocytosis. Method and Results— LRP-1 −/− macrophages displayed nearly 2-fold more TUNEL positivity compared to wild-type cells in the presence of DMEM alone or with either lipopolysaccharide or oxidized low-density lipoprotein. The survival kinase, phosphorylated Akt, was barely detectable in LRP-1 −/− cells, causing decreased phosphorylated Bad and increased cleaved caspase-3. Regardless of the apoptotic stimulation and degree of cell death, LRP-1 −/− macrophages displayed enhanced inflammation with increased IL-1β, IL-6, and tumor necrosis factor-α expression. Efferocytosis of apoptotic macrophages was reduced by 60% in LRP-1 −/− vs wild-type macrophages despite increased apolipoprotein E expression by both LRP-1 −/− phagocytes and wild-type apoptotic cells. Compared to wild-type macrophage lesions, LRP-1 −/− lesions had 5.7-fold more necrotic core with more dead cells not associated with macrophages. Conclusion— Macrophage LRP-1 deficiency increases cell death and inflammation by impairing phosphorylated Akt activation and efferocytosis. Increased apolipoprotein E expression in LRP-1 −/− macrophages suggests that the LRP-1/apolipoprotein E axis regulates the balance between apoptosis and efferocytosis, thereby preventing necrotic core formation." @default.
- W2108626579 created "2016-06-24" @default.
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- W2108626579 date "2010-04-01" @default.
- W2108626579 modified "2023-10-16" @default.
- W2108626579 title "Macrophage LRP-1 Controls Plaque Cellularity by Regulating Efferocytosis and Akt Activation" @default.
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- W2108626579 doi "https://doi.org/10.1161/atvbaha.109.202051" @default.
- W2108626579 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2845445" @default.
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