Overexpressed connective tissue growth factor in cardiomyocytes attenuates left ventricular remodeling induced by angiotensin II perfusion

• Published in: Clinical and experimental hypertension (1993) 2017-02, Vol.39 (2), p.168-174
• Main Authors: Zhang, Ying, Yan, Hua, Guang, Gong-chang, Deng, Zheng-rong
• Format: Article
• Language: English
• Subjects: Actins - drug effects; Actins - genetics; Angiotensin II; Angiotensin II - pharmacology; Animals; Blood Pressure - drug effects; Cardiomegaly - diagnostic imaging; Cardiomegaly - genetics; Cardiomegaly - pathology; cardiomyocyte; Collagen Type I - drug effects; Collagen Type I - genetics; connective tissue growth factor; Connective Tissue Growth Factor - genetics; Echocardiography; Fibrosis; Heart - diagnostic imaging; Heart - drug effects; Heart Ventricles - diagnostic imaging; Heart Ventricles - metabolism; Heart Ventricles - pathology; hypertension; Hypertension - metabolism; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; mouse; Myocardium - metabolism; Myocardium - pathology; Myocytes, Cardiac - drug effects; Myocytes, Cardiac - metabolism; overexpression; Reverse Transcriptase Polymerase Chain Reaction; Transforming Growth Factor beta - drug effects; Transforming Growth Factor beta - genetics; Vasoconstrictor Agents - pharmacology; Ventricular Remodeling - drug effects; Ventricular Remodeling - genetics
• ISSN: 1064-1963; 1525-6006
• DOI: 10.1080/10641963.2016.1226893

To evaluate the improving effects of specifically overexpressed connective tissue growth factor (CTGF) in cardiomyocytes on mice with hypertension induced by angiotensin II (AngII) perfusion, 24 transgenic mice with cardiac-restricted overexpression of CTGF (Tg-CTGF) were divided into two equal groups that were perfused with acetic acid and AngII, respectively, for 7 days. Another 24 cage-control wild-type C57BL/6 mice (NLC) were divided and treated identically. Blood pressure was detected by caudal artery cannulation. Cardiac structural and functional changes were observed by echocardiography. Cardiac fibrosis was detected by Masson staining. After AngII perfusion, blood pressures of NLC and Tg-CTGF mice, especially those of the formers, significantly increased. Compared with NLC + AngII group, Tg-CTGF + AngII group had significantly lower left ventricular posterior wall thickness at end-diastole and left ventricular posterior wall thickness at end-systole as well as significantly higher left ventricular end-systolic diameter and left ventricular end-diastolic diameter (P < 0.05). Reverse transcription-polymerase chain reaction (RT-PCR) showed that Tg-CTGF + AngII group had significantly lower collagen I, α-SMA, and TGF-β mRNA expressions in cardiac tissues (P < 0.05). Tg-CTGF can protect AngII-induced cardiac remodeling of mice with hypertension by mitigating inflammatory response. CTGF may be a therapy target for hypertension-induced myocardial fibrosis, but the detailed mechanism still needs in-depth studies.