Mi-BMSCs alleviate inflammation and fibrosis in CCl4-and TAA-induced liver cirrhosis by inhibiting TGF-β/Smad signaling

• Published in: Materials today bio 2024-04, Vol.25, p.100958-100958, Article 100958
• Main Authors: Shi, Qing, Xia, Yuhan, Wu, Minmin, Pan, Yating, Wu, Shiyi, Lin, Jiawei, Kong, Yifan, Yu, Zhijie, Zan, Xingjie, Liu, Pixu, Xia, Jinglin
• Format: Article
• Language: English
• Subjects: Bone marrow mesenchymal stem cells; Fibrosis; Full Length; Liver cirrhosis; Porous microspheres; TGF-β/Smad
• ISSN: 2590-0064; 2590-0064
• DOI: 10.1016/j.mtbio.2024.100958

Cirrhosis is an aggressive disease, and over 80 % of liver cancer patients are complicated by cirrhosis, which lacks effective therapies. Transplantation of mesenchymal stem cells (MSCs) is a promising option for treating liver cirrhosis. However, this therapeutic approach is often challenged by the low homing ability and short survival time of transplanted MSCs in vivo. Therefore, a novel and efficient cell delivery system for MSCs is urgently required. This new system can effectively extend the persistence and duration of MSCs in vivo. In this study, we present novel porous microspheres with microfluidic electrospray technology for the encapsulation of bone marrow-derived MSCs (BMSCs) in the treatment of liver cirrhosis. Porous microspheres loaded with BMSCs (Mi-BMSCs) exhibit good biocompatibility and demonstrate better anti-inflammatory properties than BMSCs alone. Mi-BMSCs significantly increase the duration of BMSCs and exert potent anti-inflammatory and anti-fibrosis effects against CCl4 and TAA-induced liver cirrhosis by targeting the TGF-β/Smad signaling pathway to ameliorate cirrhosis, which highlight the potential of Mi-BMSCs as a promising therapeutic approach for early liver cirrhosis. A 3D cell culture and cell delivery systems (Porous microsphere) encapsulated bone-mesenchymal stem cells (BMSCs) via microfluidic electrospray has excellent biocompatibility and stability, prolong retention in vivo, and significantly improve liver function, alleviate inflammation and fibrosis in CCl4-and TAA-induced liver cirrhosis by inhibiting TGF-β/Smad signaling. [Display omitted]