Figure 7.

Overexpression of miR-26a in PACs, but not myeloid cells, mitigates pancreatic injury and systemic inflammation in CER-AP

(A–F) Effects of myeloid cell-specific miR-26a overexpression (Lyz Tg) on CER-AP. Representative images (H&E; scale bar, 50 μm; magnification ×200) for pancreatic histopathology (A) and corresponding scores for edema, inflammatory cell infiltration, PAC necrosis, and their sum value (B), serum amylase and lipase (C), pancreatic mRNA markers for inflammation (D), as well as lung myeloperoxidase (MPO) activity (E) and lung alveolar membrane thickening score (F) from Lyz Tg and their WT littermates in CER-AP (50 μg/kg/h × 7 cerulein) at 12 h after disease induction. (G–N) Effects of PAC-specific miR-26a overexpression on CER-AP. Schematic showing intraperitoneal administration of tamoxifen-induced miR-26a overexpression and cerulein administration regimens (G). Representative images (H&E; scale bar, 50 μm; magnification ×200) for pancreatic histopathology (H) and corresponding scores for edema, inflammatory cell infiltration, PAC necrosis, and their sum value (I), serum amylase, lipase, and IL-6 levels (J), pancreatic mRNA markers for oxidation (K), ER stress (L), and inflammasome activation (M), and Trpc3 and Trpc6 protein levels, impaired autophagy, and inflammasome activation (N) from Ela-Tg mice and their WT littermates in CER-AP. All experiments had six to nine mice in each group except for those in western blotting analysis (n = 3).