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. Author manuscript; available in PMC: 2020 Sep 1.
Published in final edited form as: Gastroenterology. 2019 May 17;157(3):731–743. doi: 10.1053/j.gastro.2019.05.010

Figure 1.

Figure 1.

Targeted deletion of HuR in mice reduces Paneth cells and autophagy activation in the intestinal epithelium. (A) Immunostaining of Paneth cells (lysozyme-positive cells) in the small intestinal mucosa of IE-HuR−/− and control littermate mice. Red, lysozyme; and green, E-cadherin (E-cad). Scale bars, 25 μm. (B) Lysozyme fluorescence intensity per crypt in IE-HuR−/− mice compared with control littermates. Values are the means ± SEM from 5 mice. *P < 0.05 compared with littermates. (C) Growth of small intestinal organoids isolated from control littermate and IE-HuR−/− mice. (D) Immunostaining of lysozyme-positive cells in the intestinal organoids described in C. Scale bars, 100 μm. (E) Immunoblots of LC3 protiens in cultured IECs transfected with siRNA targetting HuR (siHuR) or control siRNA (C-siRNA). The levels of HuR and LC3 were examined 48 h after the transfection. (F) Effect of HuR silencing on autophagy activation induced by rapamycin in cultured IEC-6 cells. Left, immunoblots of LC3-I and LC3-II 8 h after exposure to rapamycin (50 ng/ml). Right, changes in LC3 activity at different times after treatment with rapamycin, as quantified by examining the ratio of LC3-II and LC3-I. Values are the means ± SEM (n = 3). * P < 0.05 compared with C-siRNA.