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18 results on '"Lv, Hai-tao"'

12. Hyperhomocysteinemia independently causes and promotes atherosclerosis in LDL receptor-deficient mice

Author

Guo, Hang-Yuan, Xu, Fu-Kang, Lv, Hai-Tao, Liu, Long-Bin, Ji, Zheng, Zhai, Xiao-Ya, Tang, Wei-Liang, and Chi, Ju-Fang

Subjects
Low-density lipoprotein, Hyperhomocysteinemia, Atherosclerosis, Homocysteine, Research Article
Abstract

Background Hyperhomocysteine is an independent risk factor of coronary heart disease (CHD). However, whether hyperhomocysteine affects the progression of atherosclerosis is unclear. In the present study, we examined the effect of hyperhomocysteine on the formation of atherosclerosis in low-density lipoprotein receptor-deficient (LDLr−/−) mice. Methods Forty-eight 7-week-old LDLr−/− mice were assigned to the following groups: mice fed a standard rodent diet (control group), mice fed a high-methionine diet (high-methionine group), mice fed a high-fat diet (high-fat group), and mice fed a diet high in both methionine and fat (high-methionine and high-fat group). At the age of 19, 23, and 27 weeks, four mice at each interval in every group were sacrificed. Results At the end of the study, mice did not show atherosclerotic lesions in the aortic sinus and aortic surface until 27 weeks old in the control group. However, atherosclerotic lesions developed in the other three groups at 19 weeks. The amount of atherosclerotic lesions on the aortic surface was lower in the high-methionine group than in the high-fat group (P < 0.001). Atherosclerotic lesions on the aortic surface in the high-methionine and high-fat group were the most severe. The mean area of atherosclerotic lesions in the aortic sinus compared with atherosclerotic lesions on the aortic surface was lower in the high-methionine group than in the high-fat group (P < 0.001). Atherosclerotic lesions in the aortic sinus in the high-methionine and high-fat group were the most severe. Conclusions Homocysteinemia accelerates atherosclerotic lesions and induces early atherosclerosis independently in LDLr−/− mice. Reducing the level of homocysteinemia may be beneficial for prevention and treatment of CHD.

Published
2014

17. Correlation between brachial artery flow-mediated dilation and endothelial microparticle levels for identifying endothelial dysfunction in children with Kawasaki disease

Author

Ding, Yue-Yue, Ren, Yan, Feng, Xing, Xu, Qiu-Qin, Sun, Ling, Zhang, Jian-Min, Dou, Ji-Juan, Lv, Hai-Tao, and Yan, Wen-Hua

Abstract

Background:We investigated vascular endothelial dysfunction by sonographic features of flow-mediated dilation (FMD) and circulating endothelial microparticles (EMPs) in Kawasaki disease (KD).Methods:Twenty-eight patients with KD were prospectively grouped according to stage of disease: acute, subacute, and convalescent. In addition, 28 healthy children and 28 febrile children were selected as controls. And cases in the convalescent phase were divided into two subgroups: coronary artery lesion (CAL) and no coronary lesion (NCAL). CD144+/CD42b-, CD62E+, and CD105+EMPs were measured by flow cytometry; FMD was obtained by sonography.Results:There were significant differences in FMD among the five groups. When compared with healthy controls, there were significantly greater numbers of CD144+/CD42b-, CD62E+, and CD105+EMPs and a higher proportion of CD62E+EMPs in KD patients. The proportions and numbers of CD144+/CD42b-, CD62E+, and CD105+EMPs in KD patients were not statistically different than in febrile controls. There were no significant differences in FMD and EMPs between the CAL and NCAL subgroups. There were significantly negative correlations between the values of FMD and EMPs in the three phases of KD.Conclusion:The increased levels of EMPs have significant correlation with decreased values of FMD, both of which may reflect endothelial dysfunction in child KD.

Published
2014
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18. Discovery of BMP10 as a new gene underpinning congenital heart defects.

Author

Dong BB, Li YJ, Liu XY, Huang RT, Yang CX, Xu YJ, Lv HT, and Yang YQ

Abstract

Objective: Aggregating evidence convincingly establishes the predominant genetic basis underlying congenital heart defects (CHD), though the heritable determinants contributing to CHD in the majority of cases remain elusive. In the current investigation, BMP10 was selected as a prime candidate gene for human CHD mainly due to cardiovascular developmental abnormalities in Bmp10 -knockout animals. The objective of this retrospective study was to identify a new BMP10 mutation responsible for CHD and characterize the functional effect of the identified CHD-causing BMP10 mutation., Methods: Sequencing assay of BMP10 was fulfilled in a cohort of 276 probands with various CHD and a total of 288 non-CHD volunteers. The available family members from the proband harboring an identified BMP10 mutation were also BMP10-genotyped. The effect of the identified CHD-causative BMP10 mutation on the transactivation of TBX20 and NKX2.5 by BMP10 was quantitatively analyzed in maintained HeLa cells utilizing a dual-luciferase reporter assay system., Results: A novel heterozygous BMP10 mutation, NM&#95;014482.3:c.247G>T;p.(Glu83*), was identified in one proband with patent ductus arteriosus (PDA), which was confirmed to co-segregate with the PDA phenotype in the mutation carrier's family. The nonsense mutation was not observed in 288 non-CHD volunteers. Functional analysis unveiled that Glu83*-mutant BMP10 had no transactivation on its two representative target genes TBX20 and NKX2.5 , which were both reported to cause CHD., Conclusion: These findings provide strong evidence indicating that genetically compromised BMP10 predisposes human beings to CHD, which sheds light on the new molecular mechanism that underlies CHD and allows for antenatal genetic counseling and individualized precise management of CHD., Competing Interests: None., (AJTR Copyright © 2024.)

Published
2024

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