Adenovirus-expressing miR-153-3p alleviates aortic calcification in a rat model with chronic kidney disease

腺病毒表达 miR-153-3p 可减轻慢性肾病大鼠模型中的主动脉钙化

阅读:14
作者:Fenghua Yao, Li Zhang, Zhong Yin, Bo Fu, Zhe Feng, Zongze He, Qinggang Li, Jijun Li, Xiangmei Chen

Background

Patients with chronic kidney disease (CKD) have abnormal calcification in vascular tissue that is a risk factor for cardiovascular disease. However, the specific molecular mechanisms for vascular calcification remain largely unknown. The present study aimed to determine the differentially expressed miRs and the underlying molecular mechanisms of miR-153-3p in vascular calcification induced by adenine.

Conclusion

These results suggest that increased vascular miR-153-3p expression attenuates adenine-induced aortic calcification via inhibiting osteogenic trans-differentiation in the thoracic aorta.

Methods

Differentially expressed miRs were screened using a microarray chip in the thoracic aorta. miRs and mRNA expression were measured by RT-qPCR. Protein expression was performed by western blotting analysis. Aortic calcification was confirmed by Von Kossa staining. The targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay.

Results

Our results revealed that the expression of miR-153-3p was significantly down-regulated in the thoracic aorta from adenine-fed rats compared with that of the control group. Transfection of miR-153-3p into the thoracic aorta markedly suppressed adenine-induced aortic calcification and significantly decreased the mRNA expression of ALP, OC, OSX, SOST and Runx2. Further studies indicated that Runx2 was a direct target gene of miR-153-3p, which was verified by dual luciferase reporter assay.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。