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rhIL23R-CHR/Fc融合蛋白通过下调ENST00000522718抑制Act-HaCaT细胞炎症和增殖

王黎明, 蒋小猛, 高悦, 马宇骁, 曾爱中, 郭薇

王黎明, 蒋小猛, 高悦, 马宇骁, 曾爱中, 郭薇. rhIL23R-CHR/Fc融合蛋白通过下调ENST00000522718抑制Act-HaCaT细胞炎症和增殖[J]. 中国药科大学学报, 2022, 53(6): 734-741. DOI: 10.11665/j.issn.1000-5048.20220613
引用本文: 王黎明, 蒋小猛, 高悦, 马宇骁, 曾爱中, 郭薇. rhIL23R-CHR/Fc融合蛋白通过下调ENST00000522718抑制Act-HaCaT细胞炎症和增殖[J]. 中国药科大学学报, 2022, 53(6): 734-741. DOI: 10.11665/j.issn.1000-5048.20220613
WANG Liming, JIANG Xiaomeng, GAO Yue, MA Yuxiao, ZENG Aizhong, GUO Wei. rhIL23R-CHR/Fc fusion protein inhibits Act-HaCaT inflammation and proliferation by downregulating ENST00000522718[J]. Journal of China Pharmaceutical University, 2022, 53(6): 734-741. DOI: 10.11665/j.issn.1000-5048.20220613
Citation: WANG Liming, JIANG Xiaomeng, GAO Yue, MA Yuxiao, ZENG Aizhong, GUO Wei. rhIL23R-CHR/Fc fusion protein inhibits Act-HaCaT inflammation and proliferation by downregulating ENST00000522718[J]. Journal of China Pharmaceutical University, 2022, 53(6): 734-741. DOI: 10.11665/j.issn.1000-5048.20220613

rhIL23R-CHR/Fc融合蛋白通过下调ENST00000522718抑制Act-HaCaT细胞炎症和增殖

基金项目: 国家自然科学基金资助项目(No.81973221);中国肝炎防治基金会-天晴肝病研究基金资助课题(No.TQGB20210089)

rhIL23R-CHR/Fc fusion protein inhibits Act-HaCaT inflammation and proliferation by downregulating ENST00000522718

Funds: This study was supported by the National Natural Science Foundation of China (No.81973221); and the Chinese Foundation for Hepatitis Prevention and Control——TianQing Liver Disease Research Fund Project (No.TQGB20210089)
  • 摘要: 银屑病是一种以慢性皮肤炎症为主要特征的自身免疫性疾病,其病因及发病机制尚未完全阐明。本研究在前期rhIL23R-CHR/Fc融合蛋白显著改善银屑病小鼠症状并初步阐明药理机制的基础上,利用TNF-α刺激人皮肤永生化角质形成细胞株(HaCat),建立银屑病细胞模型(Act-HaCaT),通过转录组测序并结合qRT-PCR,筛选rhIL23R-CHR/Fc融合蛋白调控Act-HaCaT细胞功能时发挥关键作用的lncRNA分子。研究结果表明,rhIL23R-CHR/Fc融合蛋白能够显著抑制Act-HaCaT细胞增殖和炎症因子产生,通过筛选得到lncRNA ENST00000522718,并发现敲低ENST00000522718能够显著抑制细胞增殖和炎症因子产生,提示ENST00000522718在银屑病的病理机制中发挥着重要作用。
    Abstract: Psoriasis is an autoimmune disease characterized by chronic skin inflammation, and its etiology and pathogenesis have not been fully elucidated to date. In the previous study, rhIL23R-CHR/Fc fusion protein had been found to significantly relieve the symptoms of psoriasis mice and the pharmacological mechanism had been initially elucidated.In this study, we established a psoriasis cell model (Act-HaCaT) using TNF-α-activated human immortalized keratinocytes (HaCat).In our current study, the lncRNA that plays a key role in the regulation of Act-HaCaT function by the rhIL23R-CHR/Fc fusion protein was screened by transcriptome sequencing combined with qRT-PCR.The results showed that rhIL23R-CHR/Fc fusion protein significantly inhibited cell proliferation and inflammatory factor production in Act-HaCaT.lncRNA ENST00000522718 was obtained by screening, and knockdown of ENST00000522718 was found to significantly inhibit cell proliferation and inflammatory factor production.Our findings suggest that ENST00000522718 plays an important role in the pathological mechanism of psoriasis.
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出版历程
  • 收稿日期:  2022-09-22
  • 修回日期:  2022-11-03
  • 刊出日期:  2022-12-24

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