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您的检索式：作者名="Chunfeng Liao"
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| 1 | Engineering an enthesis-like graft for rotator cuff repair:An approach to fabricate highly biomimetic scaffold capable of zone-specifically releasing stem cell differentiation inducers显示文摘Rotator cuff(RC)attaches to humerus across a triphasic yet continuous tissue zones(bone-fibrocartilage-tendon),termed“enthesis”.Regrettably,rapid and functional enthesis regeneration is challenging after RC tear.The existing grafts bioengineered for RC repair are insufficient,as they were engineered by a scaffold that did not mimic normal enthesis in morphology,composition,and tensile property,meanwhile cannot simultaneously stimulate the formation of bone-fibrocartilage-tendon tissues.Herein,an optimized decellularization approach based on a vacuum aspiration device(VAD)was developed to fabricate a book-shaped decellularized enthesis matrix(O-BDEM).Then,three recombinant growth factors(CBP-GFs)capable of binding collagen were synthesized by fusing a collagen-binding peptide(CBP)into the N-terminal of BMP-2,TGF-β3,or GDF-7,and zone-specifically tethered to the collagen of O-BDEM to fabricate a novel scaffold(CBP-GFs/O-BDEM)satisfying the above-mentioned requirements.After ensuring the low immunogenicity of CBP-GFs/O-BDEM by a novel single-cell mass cytometry in a mouse model,we interleaved urine-derived stem cell-sheets into this CBP-GFs/O-BDEM to bioengineer an enthesis-like graft.Its high-performance on regenerating enthesis was determined in a canine model.These findings indicate this CBP-GFs/O-BDEM may be an excellent scaffold for constructing enthesis-like graft to patch large/massive RC tears,and provide breakthroughs in fabricating graded interfacial tissue. | Can Chen Qiang Shi Muzhi Li Yang Chen Tao Zhang Yan Xu Yunjie Liao Shulin Ding Zhanwen Wang Xing Li Chunfeng Zhao Lunquan Sun Jianzhong Hu Hongbin Lu | 2022 | Bioactive Materials2022，7，10： | 4 |
| 2 | MALAT1-mediated EZH2 Recruitment to the GFER Promoter Region Curbs Normal Hepatocyte Proliferation in Acute Liver Injury显示文摘Background and Aims:The goal of this study was to investigate the mechanism by which the long noncoding RNA MALAT1 inhibited hepatocyte proliferation in acute liver injury(ALI).Methods:Lipopolysaccharide(LPS)was used to induce an ALI cellular model in HL7702 cells,in which lentivirus vectors containing MALAT1/EZH2/GFER overexpression or knockdown were introduced.A series of experiments were performed to determine their roles in liver injury,oxidative stress injury,and cell biological processes.The interaction of MALAT1 with EZH2 and enrichment of EZH2 and H3K27me3 in the GFER promoter region were identified.Rats were treated with MALAT1 knockdown or GFER overexpression before LPS induction to verify the results derived from the in vitro assay.Results:MALAT1 levels were elevated and GFER levels were reduced in ALI patients and the LPS-induced cell model.MALAT1 knockdown or GFER overexpression suppressed cell apoptosis and oxidative stress injury induced cell proliferation,and reduced ALI.Functionally,MALAT1 interacted directly with EZH2 and increased the enrichment of EZH2 and H3K27me3 in the GFER promoter region to reduce GFER expression.Moreover,MALAT1/EZH2/GFER was activated the AMPK/mTOR signaling pathway.Conclusion:Our study highlighted the inhibitory role of reduced MALAT1 in ALI through the modulation of EZH2-mediated GFER. | Li Chen Xintong Kang Xiujuan Meng Liang Huang Yiting Du Yilan Zeng Chunfeng Liao | 2023 | Journal of Clinical and Translational Hepatology2023，11，1： | 0 |
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