Introduction 3. Methods 3.1 Animal model preparation 3.2 Experiments 3.3 Data analysis 4. Results 4.1 Noninvasive blood pressure, weight loss, and cardiac weight index of rats 4.2 Von Kossa staining in the aorta 4.3 The calcium content and the activity of ALP in the aorta tissue 4.4 Masson's trichrome staining 4.5 The content of the C-reactive protein, IL-6, TNF-α and MCP-1 in serum 4.6 The content of Urotensin II and aldosterone in the aorta tissue 4.7 The change of the immunoreactivity 5. Discussion 6. Conclusions 7. Author contributions 8. Ethics approval and consent to participate 9. Acknowledgment 10. Funding 11. Conflict of interest 12. Availability of data and materials 13. References

The present study aimed to assess the role of urocortin II (UII) in the process of vascular calcification in vitro by using a calcification model, and to detect the changes in the mRNA and protein levels of associated markers in rat adventitial fibroblasts (AFs) during their phenotypic transformation to osteoblast cells，and clarify the main signal transduction pathway of UII responsible for regulating vascular calcification and AF phenotypic transformation of osteoblast cells and prove that UII was an endogenous factor promoting vascular calcification, so as to provide an effective experimental basis for the clinical regulation of related diseases caused by vascular calcification. Finally we successfully constructed the calcified cell model, found that UII was an endogenous substance regulating vascular calcification, regulated the vascular calcification by promoting apoptosis and inhibiting autophagy through up- and down-regulated Bax and Bcl-2/Beclin-1 level, and the Wnt/β-catenin signaling pathway was involved.

The present study aimed to assess the role of urocortin II (UII) in the process of vascular calcification in vitro by using a calcification model, and to detect the changes in the mRNA and protein levels of associated markers in rat adventitial fibroblasts (AFs) during their phenotypic transformation to osteoblast cells, and clarify the main signal transduction pathway of UII responsible for regulating vascular calcification and AF phenotypic transformation of osteoblast cells and prove that UII was an endogenous factor promoting vascular calcification, so as to provide an effective experimental basis for the clinical regulation of related diseases caused by vascular calcification. Finally we successfully constructed the calcified cell model, found that UII was an endogenous substance regulating vascular calcification, regulated the vascular calcification by promoting apoptosis and inhibiting autophagy through up- and down-regulated Bax and Bcl-2/Beclin-1 level, and the Wnt/β-catenin signaling pathway was involved.