Optimal time window for observation of calcific aortic valve disease in mice following catheter-induced valve injury.
10.12122/j.issn.1673-4254.2022.10.13
- Author:
Jing Xin ZENG
1
;
Shu Wen SU
1
;
Gao Peng XIAN
1
;
Qing Chun ZENG
1
;
Ding Li XU
1
Author Information
1. State Key Laboratory of Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
- Publication Type:Journal Article
- Keywords:
calcific aortic valve disease;
catheter injury;
mouse model
- MeSH:
Animals;
Mice;
Aortic Valve/metabolism*;
Calcium/metabolism*;
Mice, Inbred C57BL;
Aortic Valve Stenosis/metabolism*;
Catheters;
Osteogenesis;
Cells, Cultured
- From:
Journal of Southern Medical University
2022;42(10):1532-1538
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the optimal time window for observation of catheter-induced valve injury that mimics calcified aortic valve disease in mice.
METHODS:A catheter was inserted into the right common carotid artery of 8-week-old C57BL6 mice under ultrasound guidance, and aortic valve injury was induced using the guide wire.At 4, 8 and 16 weeks after modeling, the mice were subjected to ultrasound measurement of the heart short axial shortening rate, aortic valve peak velocity and aortic valve orifice area.Grain-Eosin staining was used to observe the changes in the thickness of the aortic valve, and calcium deposition in the aortic valve was assessed using Alizarin red staining.Immunofluorescence assay was performed to detect the expression of alkaline phosphatase (ALP) in the aortic valve.
RESULTS:At 4, 8 and 16 weeks after modeling, valve thickness (P=0.002), calcium deposition (P < 0.0001) and the expression of osteogenic protein ALP (P=0.0016) were significantly increased, but their increments were comparable at the 3 time points of observation.
CONCLUSION:In mouse models of calcific aortic valve disease induced by catheter valve injury, 4 weeks after the injury appears to be the optimal time window for observation of pathophysiological changes in the aortic valves to avoid further increase of the death rate of the mice over time.
