T-cadherin deficiency increases vascular vulnerability in T2DM through impaired NO bioactivity.
Publication/Presentation Date
1-19-2017
Abstract
BACKGROUND: Endothelial dysfunction plays a critical role in the development of type 2 diabetes (T2DM). T-cadherin (T-cad) has gained recognition as a regulator of endothelial cell (EC) function. The present study examined whether T-cad deficiency increases vascular vulnerability in T2DM.
METHODS: Vascular segments were isolated from WT or T-cad knockout mice. Endothelial function, total NO accumulation, and the expression of T-cad related proteins were determined.
RESULTS: Ach and acidified NaNO2 induced similar vasorelaxation in WT groups. T-cad KO mice exhibited normal response to acidified NaNO2, but manifested markedly reduced response to Ach. NO accumulation was also decreased in T-cad KO group. T-cad expression was reduced in WT mice fed 8 weeks of high fat diet (HFD). Furthermore, exacerbated reduction of vasorelaxation was observed in T-cad KO mice fed 8 weeks of HFD.
CONCLUSIONS: In the current study, we provide the first in vivo evidence that T-cadherin deficiency causes endothelial dysfunction in T2DM vascular segments, suggesting the involvement of T-cad deficiency in T2DM pathogenesis.
Volume
16
Issue
1
First Page
12
Last Page
12
ISSN
1475-2840
Published In/Presented At
Wang, H., Tao, L., Ambrosio, A., Yan, W., Summer, R., Lau, W. B., Wang, Y., & Ma, X. (2017). T-cadherin deficiency increases vascular vulnerability in T2DM through impaired NO bioactivity. Cardiovascular diabetology, 16(1), 12. https://doi.org/10.1186/s12933-016-0488-0
Disciplines
Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods
PubMedID
28103886
Department(s)
Administration and Leadership
Document Type
Article