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Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
Fine particulate matter promoted vascular calcification through the miR-27b-5p/HES1 signaling pathway
Ruiyang Ding1, Kanglin Yan1, Linyuan Huang1
1Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing 100069, China; Beijing Key Laboratory of environment and aging, Capital Medical University, Beijing 100069, China; Laboratory for Clinical Medicine, Capital Medical University, Beijing 100069, China.
Abstract:
Fine particulate matter (PM2.5) remains to be the leading cause of global disease burden and is linked to arterial calcification in humans. This study revealed that PM2.5 facilitated the phenotype switching of mouse aortic smooth muscle (MOVAS) cells and promoted in vitro calcification in the present of phosphate calcification medium. Mechanistic investigations revealed that PM2.5 may inhibit the transcription of miR-27b-5p in an XBP1 dependent manner, which subsequently promoted the interaction of HES1 and Runx2, eventually leading to the osteogenic transformation of MOVAS cells. More importantly, through using human induced pluripotent stem cells (hiPSCs)-derived 3D blood vessel organoids to simulate PM2.5-induced effects on the vascular system, we also observed that PM2.5 enhanced the expression of osteogenic markers, while pretreatment with miR-27b-5p mimics could significantly attenuate the phenotype switching of VSMCs and calcium deposition in the organoids. The proposed mechanisms were also confirmed by a mouse model, in which PM2.5 could promote vascular calcification, increase intima-media thickness, and interfere with vascular function in both dosage and duration-dependent manners. In summary, this study comprehensively evaluated PM2.5-induced vascular calcification and unraveled implicated mechanisms, highlighting the importance of consistent efforts in reducing PM2.5 pollution and identifying sensitive cardiovascular biomarkers.
Insights
Fine particulate matter (PM2.5) drives arterial calcification by altering smooth muscle cells and inhibiting miR-27b-5p. Reducing PM2.5 exposure is crucial for cardiovascular health.
Area of Science:
- Environmental Health
- Cardiovascular Biology
- Molecular Toxicology
Background:
- Fine particulate matter (PM2.5) is a major global health risk, linked to cardiovascular diseases.
- Arterial calcification is a key factor in vascular dysfunction and disease progression.
Purpose of the Study:
- To investigate the mechanisms by which PM2.5 induces vascular calcification.
- To explore the role of miR-27b-5p in PM2.5-mediated arterial calcification.
- To validate findings using in vitro, organoid, and in vivo models.
Main Methods:
- Utilized mouse aortic smooth muscle cells (MOVAS) and phosphate calcification medium for in vitro studies.
- Employed human induced pluripotent stem cells (hiPSCs)-derived 3D blood vessel organoids.
- Conducted experiments on a mouse model exposed to PM2.5.
Main Results:
- PM2.5 induced MOVAS cell phenotype switching and promoted calcification.
- PM2.5 inhibited miR-27b-5p via an XBP1-dependent pathway, promoting HES1/Runx2 interaction and osteogenic transformation.
- 3D organoid and mouse models confirmed PM2.5-induced vascular calcification, increased intima-media thickness, and impaired vascular function.
Conclusions:
- PM2.5 promotes vascular calcification through the miR-27b-5p/HES1/Runx2 pathway.
- miR-27b-5p mimics can mitigate PM2.5-induced vascular calcification.
- Findings underscore the need to reduce PM2.5 pollution and identify cardiovascular biomarkers.
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