1. Academic Validation
  2. Coaction of TGF-β1 and CDMP1 in BMSCs-induced laryngeal cartilage repair in rabbits

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

  • J Mater Sci Mater Med. 2020 Nov 30;31(12):130. doi: 10.1007/s10856-020-06454-x.
Linxiang Ma 1 Yonghong Zhang 1 Caihua Wang 2
Affiliations

Affiliations

  • 1 Department of Otolaryngology, Affiliated Hospital of Jining Medical University, Jining, 272029, Shandong, PR China.
  • 2 Department of Otolaryngology, Affiliated Hospital of Jining Medical University, Jining, 272029, Shandong, PR China. [email protected].
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 cartilage 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.

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