LncRNA HOTAIR promotes endometrial fibrosis by activating TGF-β1/Smad pathway
| Autor: | Yinmei Dai, Lingge Jin, Dan Lu, Liang Huang, Jing Chen, Juhong Liu, Ziwen Jiang, Yudi Zhang, Aihong Duan, Zhaohui Liu, Jianhong Wu |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Adult
0301 basic medicine Stromal cell Primary Cell Culture Biophysics Apoptosis Tissue Adhesions Smad2 Protein SMAD Biochemistry Collagen Type I Transforming Growth Factor beta1 03 medical and health sciences 0302 clinical medicine Fibrosis medicine Humans Gene silencing Smad3 Protein Cell Proliferation Uterine Diseases biology Chemistry HOTAIR General Medicine Transforming growth factor beta medicine.disease Actins Up-Regulation Antisense RNA Collagen Type I alpha 1 Chain 030104 developmental biology Gene Knockdown Techniques 030220 oncology & carcinogenesis Cell Transdifferentiation embryonic structures Cancer research biology.protein Female RNA Long Noncoding Stromal Cells Signal Transduction Transforming growth factor |
| Zdroj: | Acta Biochimica et Biophysica Sinica. 52:1337-1347 |
| ISSN: | 1672-9145 |
| Popis: | Homeobox transcript antisense RNA (HOTAIR) is a long non-coding RNA associated with a number of fibrosis-related diseases. The aim of this study was to investigate the specific role of HOTAIR in the development of endometrial fibrosis and to identify the molecular mechanisms underlying this process. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to determine the expression levels of HOTAIR in samples of intrauterine adhesion (IUA) tissue and in endometrial stromal cells (ESCs) that had been treated with transforming growth factor beta 1 (TGF-β1). Additionally, we transfected ESCs with either overexpression plasmid (pcDNA-HOTAIR) or silencing construct (si-HOTAIR) and then treated these cells with TGF-β1. We then performed RT-qPCR and western blot analysis, along with cell proliferation and apoptosis assays, to investigate the effects of HOTAIR on the transdifferentiation of ESCs into myofibroblasts. The results showed that the expression levels of HOTAIR were significantly elevated in IUA tissue and in ESCs that had been treated with TGF-β1. The overexpression of HOTAIR had a pro-fibrotic effect on ESCs, while the silencing of HOTAIR exerted an anti-fibrotic effect. Most importantly, the protein expression levels of p-Smad2 and p-Smad3 were significantly upregulated in TGF-β1-treated ESCs transfected with pcDNA-HOTAIR and were downregulated after transfection with si-HOTAIR constructs. These data indicate that HOTAIR promotes endometrial fibrosis by activating the TGF-β1/Smad signaling pathway, suggesting that the inhibition of HOTAIR may represent a promising therapeutic option for suppressing endometrial fibrosis. |
| Databáze: | OpenAIRE |
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