- 著者
- Ping Zhang Jianfang Luo Tianlong Wu Xuan Wang Fan Yang Yanhong Yu Lihe Lu Huimin Yu
- 出版者
- International Heart Journal Association
- 雑誌
- International Heart Journal (ISSN:13492365)
- 巻号頁・発行日
- vol.63, no.5, pp.928-938, 2022-09-30 (Released:2022-09-30)
- 参考文献数
- 39
- 被引用文献数
- 4
The role of endothelial injury and inflammation in atherosclerosis has been well established. miRNAs have been found to be key regulators in the development of atherosclerosis. Here we investigated whether miR-32-5p and its predicted target gene axin interactor, dorsalization associated (AIDA) are involved in endothelial injury and inflammation. Human umbilical vein endothelial cells (HUVECs) were treated with oxidized low-density lipoprotein (oxLDL) to induce endothelial injury and inflammation. AIDA was predicted to be a target gene of miR-32-5p using TargetScan software. Cell viability, migration, and angiogenesis were evaluated using Cell Counting Kit-8, wound-healing, and tube formation assays, respectively. The expression of inflammatory factors was detected using quantitative PCR, enzyme-linked immunosorbent assay, and western blot. We found that miR-32-5p expression was significantly decreased, whereas AIDA expression was significantly increased in oxLDL-treated HUVECs and the increased AIDA expression was reversed by the up-regulation of miR-32-5p. Moreover, both miR-32-5p mimic and knockdown of AIDA enhanced cell viability, promoted cell migration and angiogenesis and suppressed the expression of inflammatory factors including IL-1β, IL-6, TNF-α, ICAM-1, and VCAM-1 in oxLDL-induced HUVECs. Furthermore, miR-32-5p was verified to directly target AIDA using dual-luciferase reporter assay. Overall, these findings suggest that miR-32-5p/AIDA signal plays an important role in oxLDL-induced endothelial injury and inflammation. This study provides new insights into novel molecular mechanisms of endothelial dysfunction and atherosclerosis.
- 著者
- Qing LI Yong FAN Xiaofang SUN Yanhong YU
- 出版者
- 日本繁殖生物学会
- 雑誌
- Journal of Reproduction and Development (ISSN:09168818)
- 巻号頁・発行日
- pp.2012-109, (Released:2012-11-09)
- 被引用文献数
- 2 13
The ectopic expression of transcription factors for reprogramming human somatic cells to a pluripotent state represents a valuable resource for the development of in vitro-based models for human disease and has great potential in regenerative therapies. However, the majority of studies have used skin fibroblasts to generate induced pluripotent stem cells (iPSCs) that typically require the enforced expression of several transcription factors, thereby posing a mutagenesis risk by the insertion of viral transgenes. To reduce this risk, iPSCs have been generated with OCT4 and KLF4 from human neural stem cells that endogenously express the remaining reprogramming factors. However, human neural stem cells are rare and difficult to obtain. Here, we show that iPSCs can be generated from human amniotic fluid cells (hAFCs) with two transcription factors: OCT4 and KLF4. Furthermore, iPSCs can be readily derived from hAFCs in a feeder-free conditions, thereby eliminating the potential variability caused by using feeder cells. Our results indicate that hAFCs represent an accessible source of cells that can be reprogrammed into pluripotent stem cells with two Yamanaka factors. Therefore, hAFCs may become a preferred cell type in the future for safe reprogramming without any exogenous genetic material.