KLF15 Overexpression Protects β-Aminopropionitrile-Induced Aortic Rupture in Rodent Model via Inhibiting Connective Tissue Growth Factor

• Published in: The Thoracic and cardiovascular surgeon Vol. 65; no. 2; p. 120
• Main Authors: Zhan, Botao, Hu, Zhipeng, Chen, Jiajun, Zhu, Rui, Zhao, Hua, Yang, Junbo, Zhang, Zengwang, Nie, Ronghua
• Format: Journal Article
• Language: English
• Published: Germany 01.03.2017
• Subjects: Aminopropionitrile; Animals; Aorta - metabolism; Aorta - pathology; Aortic Aneurysm - chemically induced; Aortic Aneurysm - genetics; Aortic Aneurysm - metabolism; Aortic Aneurysm - prevention & control; Aortic Rupture - chemically induced; Aortic Rupture - genetics; Aortic Rupture - metabolism; Aortic Rupture - prevention & control; Cells, Cultured; Collagen Type I - metabolism; Collagen Type III - metabolism; Connective Tissue Growth Factor - metabolism; Dilatation, Pathologic; Disease Models, Animal; Gene Transfer Techniques; Genetic Therapy - methods; Humans; Kruppel-Like Transcription Factors - biosynthesis; Kruppel-Like Transcription Factors - genetics; Kruppel-Like Transcription Factors - metabolism; Male; Nuclear Proteins - metabolism; Rats, Sprague-Dawley; Signal Transduction; Time Factors; Transfection; Up-Regulation; Vascular Remodeling

KLF15 (Krüppel-like factor 15) was reported to be involved in a lot of cardiovascular diseases. Little is known about its role in initiation and development of aortic dissection (AD).  Samples of the human aorta were collected during AD surgery and aortic valve replacement. Lentivirus was used for i...