Figure 6
Figure 6. miR-21 suppresses the peritoneal monocyte/macrophage inflammatory response to LPS. Mice were intraperitoneally injected with endotoxin-free LNA-miR-21 inhibitor (LNA-miR-21-I) or mismatch inhibitor control (MMC) at days 1 and 3, followed by intraperitoneal injections of LPS or PBS at days 3 and 4. Peritoneal lavages were collected on day 5 at 18 or 48 hours post-LPS. Total viable CD11b+SSCAloLy6C+Ly6G− monocytes (A), CD11b+SSCAloLy6C−Ly6Glo/−F4-80+ macrophages (B), SPMs and large peritoneal macrophages (LPMs),45 (C) and the percent expression levels of the cell surface marker MHC II on the CD11b+SSCAloLy6C−Ly6Glo/-F4-80+ macrophages (D) were determined by flow cytometry. Data are representative of 2 independent experiments, 3 to 4 mice per group (error bars, ±SD; *P ≤ .05).

miR-21 suppresses the peritoneal monocyte/macrophage inflammatory response to LPS. Mice were intraperitoneally injected with endotoxin-free LNA-miR-21 inhibitor (LNA-miR-21-I) or mismatch inhibitor control (MMC) at days 1 and 3, followed by intraperitoneal injections of LPS or PBS at days 3 and 4. Peritoneal lavages were collected on day 5 at 18 or 48 hours post-LPS. Total viable CD11b+SSCAloLy6C+Ly6G monocytes (A), CD11b+SSCAloLy6CLy6Glo/−F4-80+ macrophages (B), SPMs and large peritoneal macrophages (LPMs),45  (C) and the percent expression levels of the cell surface marker MHC II on the CD11b+SSCAloLy6CLy6Glo/-F4-80+ macrophages (D) were determined by flow cytometry. Data are representative of 2 independent experiments, 3 to 4 mice per group (error bars, ±SD; *P ≤ .05).

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