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Fibronectin type III domain containing 5 attenuates NLRP3 inflammasome activation and phenotypic transformation of adventitial fibroblasts in spontaneously hypertensive rats.
Ling, Li; Chen, Dan; Tong, Ying; Zang, Ying-Hao; Ren, Xing-Sheng; Zhou, Hong; Qi, Xiao-Hong; Chen, Qi; Li, Yue-Hua; Kang, Yu-Ming; Zhu, Guo-Qing.
Affiliation
  • Ling L; Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology.
  • Chen D; Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology.
  • Tong Y; Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology.
  • Zang YH; Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology.
  • Ren XS; Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology.
  • Zhou H; Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology.
  • Qi XH; Department of Pathophysiology, Nanjing Medical University, Nanjing, Jiangsu.
  • Chen Q; Department of Pathophysiology, Nanjing Medical University, Nanjing, Jiangsu.
  • Li YH; Department of Pathophysiology, Nanjing Medical University, Nanjing, Jiangsu.
  • Kang YM; Department of Physiology and Pathophysiology, Cardiovascular Research Center, Xi'an Jiaotong University School of Medicine, Xi'an, China.
  • Zhu GQ; Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology.
J Hypertens ; 36(5): 1104-1114, 2018 05.
Article in En | MEDLINE | ID: mdl-29303830
ABSTRACT

OBJECTIVE:

Phenotypic transformation of adventitial fibroblasts is important in the pathogenesis of hypertension. This study was designed to determine whether fibronectin type III domain containing 5 (FNDC5) alleviates the phenotypic transformation of adventitial fibroblasts in hypertension and the underlying mechanisms. METHODS AND

RESULTS:

Experiments were carried out in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) and primary aortic adventitial fibroblasts. FNDC5 was downregulated and NLRP3 inflammasome was activated in aortic adventitia of SHR. FNDC5 overexpression attenuated adventitial fibroblasts phenotypic transformation, excessive synthesis and secretion of matrix components, NLRP3 inflammasome activation and inflammation in adventitial fibroblasts from SHR. Moreover, FNDC5 overexpression reduced NADPH oxidase 2 (NOX2) expression and reactive oxygen species (ROS) production in adventitial fibroblasts from SHR. Similarly, exogenous FNDC5 inhibited adventitial fibroblasts phenotypic transformation, expression of matrix components, NLRP3 inflammasome activation and NOX2 expression in adventitial fibroblasts from SHR. FNDC5 overexpression in rats attenuated phenotypic transformation, inflammation and reactive oxygen species (ROS) production in the aortic adventitia of SHR. Furthermore, FNDC5 overexpression reduced blood pressure and alleviated vascular remodeling in SHR.

CONCLUSION:

FNDC5 reduces NOX2-derived ROS production, NLRP3 inflammasome activation and phenotypic transformation in adventitial fibroblasts of SHR. FNDC5 plays a beneficial role in attenuating vascular inflammation, vascular remodeling and hypertension in SHR.
Subject(s)

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Fibronectins / Inflammasomes / Fibroblasts / NLR Family, Pyrin Domain-Containing 3 Protein / Hypertension Limits: Animals Language: En Journal: J Hypertens Year: 2018 Document type: Article

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Fibronectins / Inflammasomes / Fibroblasts / NLR Family, Pyrin Domain-Containing 3 Protein / Hypertension Limits: Animals Language: En Journal: J Hypertens Year: 2018 Document type: Article