Hyaluronic acid-curcumin conjugate suppresses the fibrotic functions of myofibroblasts from contractive joint by the PTGER2 demethylation | Zendy

Dongjie Yu | Zendy; Ze Zhuang | Zendy; Jianhua Ren | Zendy; Xuefeng Hu | Zendy; Zhe Wang | Zendy; Jieyu Zhang | Zendy; Yuansen Luo | Zendy; Kun Wang | Zendy; Ronghan He | Zendy; Yunbing Wang | Zendy

Open Access

Hyaluronic acid-curcumin conjugate suppresses the fibrotic functions of myofibroblasts from contractive joint by the PTGER2 demethylation

Author(s) -

Dongjie Yu,

Ze Zhuang,

Jianhua Ren,

Xuefeng Hu,

Zhe Wang,

Jieyu Zhang,

Yuansen Luo,

Kun Wang,

Ronghan He,

Yunbing Wang

Publication year - 2019

Publication title -

regenerative biomaterials

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.166

H-Index - 25

ISSN - 2056-3426

DOI - 10.1093/rb/rbz016

Subject(s) - curcumin , hyaluronic acid , conjugate , demethylation , chemistry , joint (building) , myofibroblast , dna demethylation , microbiology and biotechnology , biochemistry , fibrosis , anatomy , biology , pathology , dna methylation , mathematics , engineering , medicine , gene , gene expression , architectural engineering , mathematical analysis

Joint contracture is a fibrotic complication induced by joint immobilization and trauma, which is characterized as excessive myofibroblast proliferation in joint capsule. The treatments of joint contracture are unsatisfied and patients are suffered from joint dysfunction. Our previous study has shown that curcumin can inhibit myofibroblast proliferation in vitro , but the major challenge is the low aqueous solubility and biological activity of curcumin. In this study, hyaluronic acid-curcumin (HA-Cur) conjugate was synthesized to suppress myofibroblasts in joint contracture. Cells were isolated from the joint capsules of joint contracture patients and induced to active myofibroblasts by transforming growth factor-β (TGF-β). The anti-fibrotic function and mechanisms of HA-Cur were investigated by immunohistochemistry, reverse transcription-quantitative polymerase chain reaction (PCR), methylation-specific PCR, western blot, transwell migration assay and proliferation assay. Results showed that 30 μM HA-Cur significantly attenuated the fibrotic functions of myofibroblast in joint contracture in vitro by regulating the methylation of prostaglandin E receptor 2 (PTGER2) and inhibiting TGF-β signaling. This may provide a mechanism for the treatment of joint contracture, and provide a molecular target PTGER2 for therapy during the pathogenesis of joint contracture.

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