Coaction of TGF-β1 and CDMP1 in BMSCs-induced laryngeal cartilage repair in rabbits

xlomafota.13 shared this article with you from Inoreader Coaction of TGF-β1 and CDMP1 in BMSCs-induced laryngeal cartilage repair in rabbits Via Latest Results for Journal of Materials Science: Materials in Medicine Abstract Bone marrow mesenchymal stem cells (BMSCs) are well-known for tissue regeneration and bone repair. This study intended to evaluate the potential efficiency BMSCs in poly(lactide-co-glycolide) (PLGA) scaffolds for the treatment of laryngeal cartilage defects. BMSCs were isolated and identified, and added with 10 ng/mL transforming growth factor-beta1 (TGF-β1) or/and 300 ng/mL CDMP1 to coculture with PLGA scaffolds. The chondrogenic differentiation, migration, and apoptosis of BMSCs were detected under the action of TGF-β1 or/and CDMP1. After successful modeling of laryngeal cartilage defects, PLGA scaffolds were transplanted into the rabbits correspondingly. After 8 weeks, laryngeal cartilage defects were assessed. Levels of collagen II, aggrecan, Sox9, Smad2, Smad3, ERK, and JNK were detected. The TGF-β1 or/and CDMP1-induced BMSCs expressed collagen II, aggrecan, and Sox9, with enhanced cell migration and inhibited apoptosis. In addition, laryngeal carti lage defect in rabbits with TGF-β1 or/and CDMP1 was alleviated, and levels of specific cartilage matrix markers were decreased. The combined effects of TGF-β1 and CDMP1 were more significant. The TGF-β1/Smad and ERK/JNK pathways were activated after TGF-β1 or/and CDMP1 were added to BMSCs or rabbits. In summary, BMSCs and PLGA scaffolds repair laryngeal cartilage defects in rabbits by activating the TGF-β1/Smad and ERK/JNK pathways under the coaction of TGF-β1 and CDMP1. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.