|Author||Chi, Liyi ♦ Hu, Xiaojing ♦ Zhang, Wentao ♦ Bai, Tiao ♦ Zhang, Linjing ♦ Zeng, Hua ♦ Guo, Ruirui ♦ Zhang, Yanhai ♦ Tian, Hongyan|
|Source||United States Department of Energy Office of Scientific and Technical Information|
|Subject Keyword||APPLIED LIFE SCIENCES ♦ ANGIOTENSIN ♦ HYPERTENSION ♦ INHIBITION ♦ RATS|
|Abstract||Angiotensin II (AngII) is the most important component of angiotensin, which has been regarded as a major contributor to the incidence of hypertension and vascular endothelial dysfunction. The adipocytokine C1q/TNF-related protein 6 (CTRP6) was recently reported to have multiple protective effects on cardiac and cardiovascular function. However, the exact role of CTRP6 in the progression of AngII induced hypertension and vascular endothelial function remains unclear. Here, we showed that serum CTRP6 content was significantly downregulated in SHRs, accompanied by a marked increase in arterial systolic pressure and serum AngII, CRP and ET-1 content. Then, pcDNA3.1-mediated CTRP6 delivery or CTRP6 siRNA was injected into SHRs. CTRP6 overexpression caused a significant decrease in AngII expression and AngII-mediated hypertension and vascular endothelial inflammation. In contrast, CTRP6 knockdown had the opposite effect to CTRP6 overexpression. Moreover, we found that CTRP6 positively regulated the activation of the ERK1/2 signaling pathway and the expression of peroxisome proliferator-activated receptor γ (PPARγ), a recently proven negative regulator of AngII, in the brain and vascular endothelium of SHRs. Finally, CTRP6 was overexpressed in endothelial cells, and caused a significant increase in PPARγ activation and suppression in AngII-mediated vascular endothelial dysfunction and apoptosis. The effect of that could be rescued by the ERK inhibitor PD98059. In contrast, silencing CTRP6 suppressed PPARγ activation and exacerbated AngII-mediated vascular endothelial dysfunction and apoptosis. In conclusion, CTRP6 improves PPARγ activation and alleviates AngII-induced hypertension and vascular endothelial dysfunction. - Highlights: • Serum CTRP6 was significantly decreased in spontaneously hypertensive rats (SHRs). • CTRP6 positively regulated the activation of the ERK1/2 signaling pathway. • CTRP6 negatively regulates PPARγ mediated Angiotensin II (AngII) expression. • CTRP6 alleviates AngII-induced hypertension and vascular endothelial dysfunction.|
|Learning Resource Type||Article|
|Publisher Place||United States|
|Journal||Biochemical and Biophysical Research Communications|
Ministry of Human Resource Development (MHRD) under its National Mission on Education through Information and Communication Technology (NMEICT) has initiated the National Digital Library of India (NDLI) project to develop a framework of virtual repository of learning resources with a single-window search facility. Filtered and federated searching is employed to facilitate focused searching so that learners can find out the right resource with least effort and in minimum time. NDLI is designed to hold content of any language and provides interface support for leading vernacular languages, (currently Hindi, Bengali and several other languages are available). It is designed to provide support for all academic levels including researchers and life-long learners, all disciplines, all popular forms of access devices and differently-abled learners. It is being developed to help students to prepare for entrance and competitive examinations, to enable people to learn and prepare from best practices from all over the world and to facilitate researchers to perform inter-linked exploration from multiple sources. It is being developed at Indian Institute of Technology Kharagpur.
NDLI is a conglomeration of freely available or institutionally contributed or donated or publisher managed contents. Almost all these contents are hosted and accessed from respective sources. The responsibility for authenticity, relevance, completeness, accuracy, reliability and suitability of these contents rests with the respective organization and NDLI has no responsibility or liability for these. Every effort is made to keep the NDLI portal up and running smoothly unless there are some unavoidable technical issues.
Ministry of Human Resource Development (MHRD), through its National Mission on Education through Information and Communication Technology (NMEICT), has sponsored and funded the National Digital Library of India (NDLI) project.
For any issue or feedback, please write to firstname.lastname@example.org