Tissue Eng Regen Med.  2021 Aug;18(4):641-650. 10.1007/s13770-021-00358-9.

Effects of Androgen Receptor Overexpression on Chondrogenic Ability of Rabbit Articular Chondrocytes

Affiliations
  • 1College and Hospital of Stomatology, Key Laboratory of Oral Diseases Research of Anhui Province, Anhui Medical University, Hefei 230032, China
  • 2Department of Oral Surgery, Shanghai Key Laboratory of Stomatology, National Clinical Research Center of Stomatology, Ninth People’s Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai 200011, China
  • 3Department of Dental Implantology, College and Hospital of Stomatology, Anhui Medical University, Hefei 230032, China

Abstract

BACKGROUND
The role of sex hormones and their receptors has drawn much attention in the process of cartilage regeneration. This study aimed to investigate the effect of androgen receptor (AR) on the chondrogenic ability of articular chondrocytes and the related mechanism.
METHODS
Articular chondrocytes were isolated, cultured, identified by toluidine blue staining and then transduced with lentivirus carrying the AR gene. The cell viability was determined using Cell Counting Kit-8, and cell apoptosis was assessed by flow cytometry analysis. The effects of AR overexpression on the expression of cartilage-specific proteins and some signalling molecules were evaluated by real-time PCR and Western blotting. Using 24 New Zealand rabbits, the regeneration of rabbit articular cartilage defects was further investigated in vivo and evaluated histologically.
RESULTS
The overexpression of AR significantly reduced the apoptosis rate of chondrocytes but did not affect their proliferation. The overexpression of AR also promoted the expression of Sry-related HMG box 9, collagen II and aggrecan, decreased the expression of matrix metalloproteinase-13, and downregulated p-S6 and RICTOR. The experimental group with AR-overexpressing chondrocytes exhibited superior regeneration of cartilage defects.
CONCLUSION
AR overexpression can maintain the phenotype of chondrocytes and promote chondrogenesis in vitro and in vivo. mTOR-related signalling was inhibited.

Keyword

Androgen receptor; Articular chondrocytes; Chondrogenesis; Tissue engineering
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