دورية أكاديمية

Effect of Salusin-ß on Peroxisome Proliferator-Activated Receptor Gamma Gene Expression in Vascular Smooth Muscle Cells and its Possible Mechanism

التفاصيل البيبلوغرافية
العنوان: Effect of Salusin-ß on Peroxisome Proliferator-Activated Receptor Gamma Gene Expression in Vascular Smooth Muscle Cells and its Possible Mechanism
المؤلفون: XiaoLe Xu, Mengzi He, Tingting Liu, Yi Zeng, Wei Zhang
المصدر: Cellular Physiology and Biochemistry, Vol 36, Iss 6, Pp 2466-2479 (2015)
بيانات النشر: Cell Physiol Biochem Press GmbH & Co KG, 2015.
سنة النشر: 2015
المجموعة: LCC:Physiology
LCC:Biochemistry
مصطلحات موضوعية: Smooth muscle cells, Signal transduction, Vascular biology, Salusin-β, Physiology, QP1-981, Biochemistry, QD415-436
الوصف: Background/Aims: salusin-ß is considered to be a potential pro-atherosclerotic factor. Regulation and function of vascular smooth muscle cells (VSMCs) are important in the progression of atherosclerosis. Peroxisome proliferator-activated receptor gamma (PPARγ) exerts a vascular protective role beyond its metabolic effects. Salusin-ß has direct effects on VSMCs. The aim of the present study was to assess the effect of salusin-ß on PPARγ gene expression in primary cultured rat VSMCs. Methods: Western blotting analysis, real-time PCR and transient transfection approach were used to determine expression of target proteins. Specific protein knockdown was performed with siRNA transfection. Cell proliferation was determined by 5-bromo-2'-deoxyuridine incorporation. The levels of inflammation indicators interleukin-6 (IL-6) and tumor necrosis factor-a (TNF-a) were determined using enzyme-linked immunosorbent assay. Results: Salusin-ß negatively regulated PPARγ gene expression at protein, mRNA and gene promoter level in VSMCs. The inhibitory effect of salusin-ß on PPARγ gene expression contributed to salusin-ß-induced VSMCs proliferation and inflammation in vitro. IγBa-NF-γB activation, but not NF-γB p50 or p65, mediated the salusin-ß-induced inhibition of PPARγ gene expression. Salusin-ß induced nuclear translocation of histone deacetylase 3 (HDAC3). HDAC3 siRNA prevented salusin-ß-induced PPARγ reduction. Nuclear translocation of HDAC3 in response to salusin-ß was significantly reversed by an IγBa inhibitor BAY 11-7085. Furthermore, IγBa-HDAC3 complex was present in the cytosol of VSMCs but interrupted after salusin-ß treatment. Conclusion: IγBa-HDAC3 pathway may contribute to salusin-ß-induced inhibition of PPARγ gene expression in VSMCs.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1015-8987
1421-9778
Relation: http://www.karger.com/Article/FullText/430207; https://doaj.org/toc/1015-8987; https://doaj.org/toc/1421-9778
DOI: 10.1159/000430207
URL الوصول: https://doaj.org/article/891c51954bd54e0fa2dcfceb96cd52f0
رقم الأكسشن: edsdoj.891c51954bd54e0fa2dcfceb96cd52f0
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:10158987
14219778
DOI:10.1159/000430207