ArticleArchives of microbiology2025
Inhibition of TGF-β1 induced epithelial-mesenchymal transition in bovine mammary epithelial cells by 6BIO.
Article in Archives of microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Mastitis is a common pathological condition in dairy cattle. If not promptly and effectively treated, it can progress to chronic subclinical mastitis, which is characterized by fibrosis of mammary gland tissue and results in a marked decline in both milk yield and quality. During chronic inflammation, transforming growth factor-β1 (TGF-β1) is often overexpressed, driving epithelial-mesenchymal transition (EMT) and subsequent tissue fibrosis. However, the molecular mechanisms by which TGF-β1 induces EMT in bovine mammary epithelial cells (BMECs) remain poorly understood. The compound 6-bromo-indirubin 3'-oxime (6BIO) is known for its anti-inflammatory, antibacterial, and anti-proliferative activities, but its role in EMT regulation has not been fully defined. Using primary BMEC cultures, this study examined the regulatory function of TGF-β1 in EMT induction and evaluated the modulatory effects of 6BIO on cell morphology, inflammatory responses, and EMT progression. Results showed that TGF-β1 triggered inflammation in BMECs, promoted their phenotypic transition to an interstitial state, induced EMT, and activated the TGF-β/Smad signaling pathway. In contrast, 6BIO inhibited this phenotypic transition, suppressed TGF-β1-induced EMT, and blocked TGF-β/Smad activation. Additionally, 6BIO directly interacted with Smad3 proteins. Overall, these findings indicate that aberrant TGF-β1 upregulation promotes EMT in BMECs, whereas 6BIO counteracts this process through interaction with Smad3. This study provides new insights into strategies for preventing and managing chronic subclinical mastitis and establishes a basis for developing anti-EMT therapeutic agents.
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