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

Hui Liu; Shoumei Xuan; Zhoujing Zhang; Kuang Gu; Duohong Zou; Jiacai He; Yong Zhou

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자료유형: 학술저널

저자정보: Hui Liu (College and Hospital of Stomatology Anhui Medical University) Shoumei Xuan (College and Hospital of Stomatology Anhui Medical University) Zhoujing Zhang (College and Hospital of Stomatology Anhui Medical University) Kuang Gu (College and Hospital of Stomatology Anhui Medical University) Duohong Zou (National Clinical Research Center of Stomatology Ninth People’s Hospital) Jiacai He (College and Hospital of Stomatology Anhui Medical University) Yong Zhou (College and Hospital of Stomatology Anhui Medical University)

저널정보: 한국조직공학과 재생의학회 조직공학과 재생의학 조직공학과 재생의학 제18권 제4호

발행연도: 2021.1

수록면: 641 - 650 (10page)

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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.

#Androgen receptor Articular chondrocytes Chondrogenesis Tissue engineering

참고문헌 (24)

참고문헌 신청

Charlier E / 2019 / Chondrocyte dedifferentiation and osteoarthritis(OA) / Biochem Pharmacol 165:49~65

Abramoff B / 2020 / Osteoarthritis : pathology, diagnosis, and treatment options / Med Clin North Am 104:293~311

Huang K / 2018 / Cartilage tissue regeneration : the roles of cells, stimulating factors and scaffolds / Curr Stem Cell Res Ther 13:547~567

Fan DX / 2018 / 17beta-estradiol on the Expression of G-protein coupled estrogen receptor(GPER/GPR30)mitophagy, and the PI3K/Akt Signaling pathway in ATDC5 chondrocytes in vitro / Med Sci Monit 24:1936~1947

Shi S / 2017 / The effect of estradiol on the growth plate chondrocytes of limb and spine from postnatal mice in vitro : the role of estrogen-receptor and estradiol concentration / Int J Biol Sci 13:100~109

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