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Your search keyword '"Zhang, Luankun"' showing total 4 results
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4 results on '"Zhang, Luankun"'

1. RIP140 triggers foam-cell formation by repressing ABCA1/G1 expression and cholesterol efflux via liver X receptor.

Author

He, Yanhong, Zhang, Luankun, Li, Zhuoming, Gao, Hui, Yue, Zhongbao, Liu, Zhiping, Liu, Xueping, Feng, Xiaojun, and Liu, Peiqing

Subjects
*RECEPTOR-interacting proteins, *GENE expression, *CHOLESTEROL, *LIPID metabolism, *C-terminal binding proteins, *PEROXISOME proliferator-activated receptors
Abstract

Receptor-interacting protein 140 (RIP140) is a multifunctional coregulator of lipid metabolism and inflammation. However, the potential role of RIP140 in atherosclerosis remains unknown. The present study investigated the impact of RIP140 on foam cell formation, a critical step in pathogenesis of atherosclerosis. The expression of RIP140 was increased in foam cells. RIP140 overexpression resulted in decreased cholesterol efflux in macrophages and their concomitant differentiation into foam cells. Moreover, RIP140 negatively regulated the macrophage expression of ATP-binding cassette transporters A1 and G1 (ABCA1/G1), by suppressing the expression and activity of liver X receptor (LXR). These findings shed light onto the contribution of RIP140 to the development and progression of atherosclerosis, and suggest a novel therapeutic target for the treatment of atherosclerosis. [ABSTRACT FROM AUTHOR]

Published
2015
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2. The p65 subunit of NF-κB involves in RIP140-mediated inflammatory and metabolic dysregulation in cardiomyocytes.

Author

Zhang, Luankun, Chen, Yanfang, Yue, Zhongbao, He, Yanhong, Zou, Jian, Chen, Shaorui, Liu, Min, Chen, Xi, Liu, Zhiping, Liu, Xueping, Feng, Xiaojun, Li, Min, and Liu, Peiqing

Subjects
*TRANSCRIPTION factors, *NF-kappa B, *METABOLIC disorders, *HEART cells, *INFLAMMATION, *LABORATORY rats
Abstract

Highlights: [•] Elevated NF-κB activity in neonatal rat cardiomyocytes overexpressing RIP140. [•] RIP140 impacts proinflammatory response of cardiomyocytes via p65-NF-κB pathway. [•] p65-NF-κB is involved in RIP140-induced metabolic dysregulation in cardiomyocytes. [ABSTRACT FROM AUTHOR]

Published
2014
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3. C/EBPβ knockdown protects cardiomyocytes from hypertrophy via inhibition of p65-NFκB.

Author

Zou, Jian, Li, Hong, Chen, Xi, Zeng, Siyu, Ye, Jiantao, Zhou, Changhua, Liu, Min, Zhang, Luankun, Yu, Na, Gan, Xiaohong, Zhou, Houfeng, Xian, Zhiwei, Chen, Shaorui, and Liu, Peiqing

Subjects
*HEART cells, *HYPERTROPHY, *NF-kappa B, *ENZYME inhibitors, *IN vitro studies, *CHROMOSOMAL translocation, *DNA-binding proteins
Abstract

Highlights: [•] C/EBPβ expression is upregulated in response to hypertrophic stimulation in vitro and in vivo. [•] C/EBPβ knockdown protects cardiomyocytes from hypertrophy. [•] C/EBPβ knockdown reduced the nuclear translocation of p65-NFκB, and diminished NFκB-DNA binding activity. [ABSTRACT FROM AUTHOR]

Published
2014
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4. Salvianolic acid B protects cardiomyocytes from angiotensin II-induced hypertrophy via inhibition of PARP-1.

Author

Liu, Min, Ye, Jiantao, Gao, Si, Fang, Wei, Li, Hong, Geng, Biao, Zou, Jian, Chen, Xi, Chen, Shaorui, Zhang, Luankun, Yue, Zhongbao, Ma, Yunzi, Gao, Hui, Li, Zhuoming, and Liu, Peiqing

Subjects
*HEART cells, *ANGIOTENSIN II, *CARDIAC hypertrophy, *ANTIOXIDANTS, *ATRIAL natriuretic peptides, *NAD (Coenzyme)
Abstract

Highlights: [•] Salvianolic acid B (SalB) protected cardiomyocytes from AngII-induced hypertrophy. [•] SalB’ anti-hypertrophy was partly attributed to its inhibition on PARP-1. [•] SalB prevented the depletion of cellular NAD+ induced by AngII. [•] SalB’s antioxidant effect might contribute to the inhibition of PARP-1. [ABSTRACT FROM AUTHOR]

Published
2014
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