Musashi2 binds TGFβR1 regulates mastitis via TGFβ/Smad signaling pathway in dairy cows

Abstract

Objective: Bacteria-induced mastitis is characterized by mammary pain, swelling of the mammary glands, and decreased milk production and quality in cows. Reducing the negative effects of inflammation is a challenge, and the regulatory mechanism of the inflammatory response in mammary epithelial cells is not yet clear. Results: Our results indicated that the RNA-binding protein Musashi2 (Msi2) regulates the inflammatory response and the blood-milk barrier in mastitis. Msi2 is commonly enriched in stem cells and tumor cells. We found that Msi2 expression was upregulated during mastitis. Silencing Msi2 in BMECs and mice increased inflammatory factors and tight junctions. Transcriptional profiling analysis revealed that Msi2 silencing increased transforming growth factor-beta (TGFβ) signaling. RNA-interacting protein immunoprecipitation assays demonstrated that Msi2 could affect the translation of transforming growth factor-beta receptor 1 (TGFβR1), thereby affecting TGFβ signaling. Overall, Msi2 silencing reduced inflammatory reactions and repaired the blood-milk barrier during mastitis Conclusions: Our findings indicate that Msi2 plays an important role in mastitis by regulating the TGFβ signaling pathway. A decrease in Msi2 can reduce the negative effects of mastitis by inhibiting the expression of inflammatory factors and increasing tight junction proteins.