Long Non-coding RNA DANCR Regulates the Proliferation and Migration of Human Adipose-derived Mesenchymal Stromal Cells in Inflammation Conditions

被引:0
|
作者
Yan, Ran [1 ]
Dong, Ping [1 ]
Yang, Zhigang [1 ]
Cao, Rui [1 ]
Xiao, Ran [1 ,2 ]
Liu, Xia [1 ,2 ]
机构
[1] Chinese Acad Med Sci, Res Ctr Plast Surg Hosp, Peking Union Med Coll, Beijing, Peoples R China
[2] Chinese Acad Med Sci, Key Lab Reconstruct Superficial Tissues & Organs, Peking Union Med Coll, Beijing, Peoples R China
基金
中国国家自然科学基金;
关键词
DANCR; dexamethasone; hASC; long non-coding RNA; migration; proliferation; TNF-alpha; STEM-CELLS; OSTEOGENIC DIFFERENTIATION; DEXAMETHASONE; ACTIVATION; EXOSOMES;
D O I
10.2174/011574888X290779240521130244
中图分类号
Q813 [细胞工程];
学科分类号
摘要
Background Mesenchymal stromal cells (MSCs) and Dexamethasone (Dex) are both effective methods to treat inflammatory diseases. However, the interaction between inflammatory factors, Dex, and MSCs in repair is not fully understood. The purpose of this study is to clarify the effects and mechanisms of glucocorticoids on the tissue repair characteristics of MSCs in an inflammatory environment.Methods This is an experimental study. Human adipose-derived mesenchymal stromal cells (hASCs) were cultured, and Long non-coding RNA (lncRNA) differentiation antagonizing non-protein coding RNA (DANCR) expression was detected after treatment with Dex and inflammation factors. Additionally, DANCR was knockdown or overexpressed before Dex or tumor necrosis factor-alpha (TNF-alpha) treatments, respectively. hASC proliferation, cell cycle, and migration ability were analyzed to evaluate the effects of DANCR in hASCs treated with Dex or TNF-alpha. Nuclear factor-kB (NF-kappa B) pathway inhibitors were used to clarify the signal pathway that DANCR involved. All data are presented as the mean +/- standard deviation. The two-tailed Student's t-test or one-way analysis of variance (ANOVA) was used to determine the statistical differences between groups.Results Dex decreased the proliferation and migration of hASCs and upregulated DANCR expression in a dosage-dependent relationship. The knockdown of DANCR reversed Dex's repression of hASC proliferation. Moreover, DANCR was decreased by inflammatory cytokines, and overexpressing DANCR alleviated the promotion effects of TNF-alpha on hASC proliferation and migration. Furthermore, mechanistic investigation validated that DANCR was involved in the NF-kappa B signaling pathway.Conclusions We identified a lncRNA, DANCR, that was involved in Dex and inflammation-affected hASC proliferation and migration. Dex reduced the proliferation and migration of hASCs through DANCR while exerting its anti-inflammatory effects. Thus, it is suggested to avoid the simultaneous application of hASCs and steroids in clinical practice. These results enrich our understanding of the versatile function of lncRNAs in the crosstalk of inflammation conditions and MSCs.
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页数:12
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