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Background. Intestinal fibrosis, one of the complications of inflammatory bowel disease (IBD), is associated with fistula and intestinal stricture formation. There are currently no treatments for fibrosis. Mesenchymal stem cell-derived exosomes have been proven to exert inhibitory and reversal effects in IBD and other organ fibrosis. In this study, we explored the role of human umbilical cord mesenchymal stem cell-derived exosomes (hucMSC-Ex) in IBD-related fibrosis and its associated mechanism to provide new ideas for the prevention and treatment of IBD-related intestinal fibrosis. Methods. We established a DSS-induced mouse IBD-related intestinal fibrosis model and observed the effect of hucMSC-Ex on the mouse model. We also used the TGF-induced human intestinal fibroblast CCD-18Co to observe the role of hucMSC-Ex in the proliferation, migration, and activation of intestinal fibroblasts. Having observed that the extracellular-signal-regulated kinase (ERK) pathway in intestinal fibrosis can be inhibited by hucMSC-Ex, we treated intestinal fibroblasts with an ERK inhibitor to emphasize the potential target of ERK phosphorylation in the treatment of IBD-associated intestinal fibrosis. Results. In the animal model of IBD-related fibrosis, hucMSC-Ex alleviated inflammation-related fibrosis as evident in the thinning of the mice’s intestinal wall and decreased expression of related molecules. Moreover, hucMSC-Ex inhibited TGF-β-induced proliferation, migration, and activation of human intestinal fibroblasts, and ERK phosphorylation played a key role in IBD-associated fibrosis. The inhibition of ERK decreased the expression of fibrosis-related indicators such as α-SMA, fibronectin, and collagen I. Conclusion. hucMSC-Ex alleviates DSS-induced IBD-related intestinal fibrosis by inhibiting profibrotic molecules and intestinal fibroblast proliferation and migration by decreasing ERK phosphorylation.

Previous studies have revealed that microRNA (miR)-150 can act as an oncomiR or a tumor suppressor in numerous types of hematological malignancy and solid tumor. However, the function of miR-150 in papillary thyroid carcinoma (PTC) remains elusive. The present study aimed to investigate the function of miR-150 in PTC and its underlying molecular mechanism. The expression of miR-150 was identified to be significantly downregulated, whereas that of mucin (MUC)4 was significantly upregulated in PTC tissues and cell lines compared with corresponding controls. Further experiments demonstrated that MUC4 is a direct target of miR-150. PTC cell proliferation and capacity for migration and invasion decreased following miR-150 overexpression. It was also demonstrated that miR-150-mediated MUC4 downregulation was associated with an accompanying decrease in human epidermal growth factor receptor 2, as well as its phosphorylated form, resulting in suppressed activation of downstream signaling. In conclusion, the present study demonstrated that miR-150 may serve a key function in suppressing the malignant growth and aggressive behavior of PTC cells through the downregulation of MUC4. These findings may provide a novel approach for diagnostic and therapeutic strategies for PTC.