rhIL23R-CHR/Fc fusion protein inhibits Act-HaCaT inflammation and proliferation by downregulating ENST00000522718
10.11665/j.issn.1000-5048.20220613
- VernacularTitle:rhIL23R-CHR/Fc融合蛋白通过下调ENST00000522718抑制Act-HaCaT细胞炎症和增殖
- Author:
Liming WANG
1
;
Xiaomeng JIANG
;
Yue GAO
;
Yuxiao MA
;
Aizhong ZENG
;
Wei GUO
Author Information
1. 中国药科大学生命科学与技术学院
- Publication Type:Journal Article
- Keywords:
lncRNA;
rhIL23R-CHR/Fc fusion protein;
proliferation;
inflammatory factor
- From:
Journal of China Pharmaceutical University
2022;53(6):734-741
- CountryChina
- Language:Chinese
-
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.
