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| Liu,Guo; Zhang,Wenhao. |
| Excessive exposure to ultraviolet (UV) rays can cause damage of the skin and may induce cancer, immunosuppression, photoaging, and inflammation. The long non-coding RNA (lncRNA) HOX antisense intergenic RNA (HOTAIR) is involved in multiple human biological processes. However, its role in UVB-induced keratinocyte injury is unclear. This study was performed to investigate the effects of HOTAIR in UVB-induced apoptosis and inflammatory injury in human keratinocytes (HaCaT cells). Quantitative real-time polymerase chain reaction was performed to analyze the expression levels of HOTAIR, PKR, TNF-α, and IL-6. Cell viability was measured using trypan blue exclusion method and cell apoptosis using flow cytometry and western blot. ELISA was used to measure the... |
| Tipo: Info:eu-repo/semantics/article |
Palavras-chave: HOTAIR; UVB-induced apoptosis; Inflammatory injury; PKR; Keratinocytes. |
| Ano: 2018 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2018000800607 |
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| Chen,Honglei; Zhang,Zhixu; Zhang,Li; Wang,Junzhi; Zhang,Minghui; Zhu,Bin. |
| MicroRNAs (miRNAs) have been reported to be associated with heart valve disease, which can be caused by inflammation. This study aimed to investigate the functional impacts of miR-27a on TNF-α-induced inflammatory injury in human mitral valve interstitial cells (hMVICs). hMVICs were subjected to 40 ng/mL TNF-α for 48 h, before which the expressions of miR-27a and NELL-1 in hMVICs were altered by stable transfection. Trypan blue staining, BrdU incorporation assay, flow cytometry detection, ELISA, and western blot assay were performed to detect cell proliferation, apoptosis, and the release of proinflammatory cytokines. We found that miR-27a was lowly expressed in response to TNF-α exposure in hMVICs. Overexpression of miR-27a rescued hMVICs from... |
| Tipo: Info:eu-repo/semantics/article |
Palavras-chave: MiR-27a; Heart valve disease (HVD); Human mitral valve interstitial cell (hMVIC); TNF-α; Inflammatory injury; NELL-1. |
| Ano: 2018 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2018000600603 |
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