Thorac Cardiovasc Surg 2017; 65(02): 120-125
DOI: 10.1055/s-0035-1566743
Original Cardiovascular
Georg Thieme Verlag KG Stuttgart · New York

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

Botao Zhan
1  Department of Cardio-thoracic Surgery, Xiangyang Central Hospital, Hubei University of Art and Science, Hubei Province, China
,
Zhipeng Hu
1  Department of Cardio-thoracic Surgery, Xiangyang Central Hospital, Hubei University of Art and Science, Hubei Province, China
,
Jiajun Chen
1  Department of Cardio-thoracic Surgery, Xiangyang Central Hospital, Hubei University of Art and Science, Hubei Province, China
,
Rui Zhu
2  Department of Cardiology, Xiangyang Central Hospital, Hubei University of Art and Science, Hubei Province, China
,
Hua Zhao
1  Department of Cardio-thoracic Surgery, Xiangyang Central Hospital, Hubei University of Art and Science, Hubei Province, China
,
Junbo Yang
1  Department of Cardio-thoracic Surgery, Xiangyang Central Hospital, Hubei University of Art and Science, Hubei Province, China
,
Zengwang Zhang
1  Department of Cardio-thoracic Surgery, Xiangyang Central Hospital, Hubei University of Art and Science, Hubei Province, China
,
Ronghua Nie
1  Department of Cardio-thoracic Surgery, Xiangyang Central Hospital, Hubei University of Art and Science, Hubei Province, China
› Author Affiliations
Further Information

Publication History

18 June 2015

26 September 2015

Publication Date:
24 November 2015 (online)

Abstract

Background 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).

Methods Samples of the human aorta were collected during AD surgery and aortic valve replacement. Lentivirus was used for in vitro and in vivo KLF15 overexpression in BAPN (β-aminopropionitrile)–induced rat AD models. The survival times were recorded and compared between the two groups. Autopsy was used for confirming aorta rupture in rat models. qPCR analyses were used for detecting gene expression whereas Western blot and immunostaining were used for detecting protein expression when necessary.

Results KLF15 expression was much lower in the aorta walls of AD group patients than the control group subjects. The survival curve showed that the survival time of AD models was prolonged after KLF15 overexpression. qPCR and Western blot showed that connective tissue growth factors (CTGFs) were significantly downregulated in the rat aortas. After KLF15 overexpression in aortic adventitial fibroblasts, the KLF15 mRNA was increased whereas CTGF and its target gene collagens I and III were downregulated. Immunofluorescence staining also showed a decrease in CTGF, collagen I, and III. Lenti-control did not induce a significant change of KLF15, CTGF, collagen I, and III expressions.

Conclusions KLF15 is involved in the mechanism of AD formation in human. Overexpression of KLF15 can partially rescue the aorta remodeling and AD formation in animal models. Our research highlighted a potential of KLF15 to serve as a new therapy target of AD.