Inhibiting microRNA-7 Expression Exhibited a Protective Effect on Intestinal Mucosal Injury in TNBS-Induced Inflammatory
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ORIGINAL ARTICLE
Inhibiting microRNA-7 Expression Exhibited a Protective Effect on Intestinal Mucosal Injury in TNBS-Induced Inflammatory Bowel Disease Animal Model Jing Guo,1 Li-juan Yang,2 Mei Sun,1 and Ling-fen Xu
1,3
This study aimed to explore the expression and correlation of microRNA-7 (miR-7) and trefoil factor 3 (TFF3) genes and proteins in inflammatory bowel disease (IBD) mouse models and to elucidate the effect of miR-7 inhibition in the intestinal mucosa in IBD models. A TNBS-induced IBD mouse model was established. Changes in intestinal inflammation were observed by HE staining, and the expression levels of miR-7 and TFF3 were detected by RT-PCR. After miRNA-antagomir injection, the degree of colonic tissue damage and the expression levels of miR-7 and TFF3 in intestinal tissues were compared. TNBS-induced IBD mice showed significant weight loss, significantly decreased disease activity index (DAI), and a significantly increased pathological damage score. miR-7 was highly expressed in the colon tissue of IBD mice, and TFF3 was downregulated. Inhibition of the expression of miR-7 improved the stool characteristics and fecal occult blood (OB) of IBD mice, significantly increased the expression of TFF3 protein, and decreased the pathological damage scores. In the IBD mouse model, miR-7 posttranscriptionally regulates TFF3. The inhibition of miR-7 expression improves some clinical manifestations of IBD mice, reduces the pathological damage of the intestinal mucosa, and shows a protective effect in IBD.
Abstract—
KEY WORDS: microRNA-7; trefoil factor 3; inflammatory bowel disease; miRNA antagomir.
INTRODUCTION
1
Department of Pediatrics, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang, 110004, Liaoning, People’s Republic of China 2 Dalian Children’s Hospital, Dalian, 116000, Liaoning, People’s Republic of China 3 To whom correspondence should be addressed at Department of Pediatrics, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang, 110004, Liaoning, People’s Republic of China. E-mail: [email protected]
Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is a recurrent chronic nonspecific bowel inflammation with a complex etiology. Approximately 25% of IBD patients develop the condition during adolescence (< 16 years), and studies have shown that the incidence of IBD in children is increasing annually [1]. IBD has chronic and prolonged clinical features and recurrent episodes. There is a lack of early monitoring methods and effective
0360-3997/19/0000-0001/0 # 2019 Springer Science+Business Media, LLC, part of Springer Nature
Guo, Yang, Sun, and Xu prevention and treatment measures, which seriously affects the growth and quality of life of patients. At present, the pathogenesis of IBD remains unclear but is generally believed to be related to genetic susceptibility, infection, environmental factors, intestinal flora imbalance, and immune dysfunction. Intestinal mucosal damage caused by an excessive
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