Parathyroid hormone accelerates decompensation following left ventricular hypertrophy.
10.3858/emm.2010.42.1.006
- Author:
Hyeseon CHA
1
;
Hyeon Joo JEONG
;
Seung Pil JANG
;
Joo Yeon KIM
;
Dong Kwon YANG
;
Jae Gyun OH
;
Woo Jin PARK
Author Information
1. Global Research Laboratory and Department of Life Science, Gwangju Institute of Science and Technology, Gwangju 500-712, Korea. wjpark@gist.ac.kr
- Publication Type:Original Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
- Keywords:
fibrosis;
heart failure;
hypertrophy, left ventricular;
parathyroid hormone
- MeSH:
Animals;
Blotting, Western;
Echocardiography;
Hypertrophy, Left Ventricular/*drug therapy/pathology;
Male;
Mice;
Mice, Inbred C57BL;
Parathyroid Hormone/pharmacology/*therapeutic use;
Phosphorylation/drug effects;
Random Allocation;
Reverse Transcriptase Polymerase Chain Reaction;
Smad2 Protein/metabolism
- From:Experimental & Molecular Medicine
2010;42(1):61-68
- CountryRepublic of Korea
- Language:English
-
Abstract:
Parathyroid hormone (PTH) treatment was previously shown to improve cardiac function after myocardial infarction by enhancing neovascularization and cell survival. In this study, pressure overload-induced left ventricular hypertrophy (LVH) was induced in mice by transverse aortic banding (TAB) for 2 weeks. We subsequently evaluated the effects of a 2-week treatment with PTH or saline on compensated LVH. After another 4 weeks, the hearts of the mice were analyzed by echocardiography, histology, and molecular biology. Echocardiography showed that hearts of the PTH-treated mice have more severe failing phenotypes than the saline-treated mice following TAB with a greater reduction in fractional shortening and left ventricular posterior wall thickness and with a greater increase in left ventricular internal dimension. Increases in the heart weight to body weight ratio and lung weight to body weight ratio following TAB were significantly exacerbated in PTH-treated mice compared to saline-treated mice. Molecular markers for heart failure, fibrosis, and angiogenesis were also altered in accordance with more severe heart failure in the PTH-treated mice compared to the saline-treated mice following TAB. In addition, the PTH-treated hearts were manifested with increased fibrosis accompanied by an enhanced SMAD2 phosphorylation. These data suggest that the PTH treatment may accelerate the process of decompensation of LV, leading to heart failure.
