Left ventricular hypertrophy in mice with a cardiac-specific overexpression of interleukin-1.
Recent studies have identified the importance of proinflammatory cytokines in the development of left ventricular (LV) hypertrophy. However, the precise role of interleukin-1 (IL-1), one of the major proinflammatory cytokines, in the myocardium is not fully understood. In this study, we investigated the pathophysiological consequences of cardiac expression of IL-1 in vivo. We generated mice with a cardiac-specific overexpression of human IL-1alpha. We then analyzed their heart morphology and functions. Histological and echocardiographic analyses revealed concentric LV hypertrophy with preserved LV systolic function in the mice. Our results suggest that myocardial expression of IL-1 is sufficient to cause LV hypertrophy.
Internal Medicine-1, National Defense Medical College, 3-2 Namiki Tokorozawa Saitama, 359-0042, Japan.
Kenichiro
K
Nishikawa
Mikoto
M
Yoshida
Masatoshi
M
Kusuhara
Norio
N
Ishigami
Kikuo
K
Isoda
Kohji
K
Miyazaki
Fumitaka
F
Ohsuzu
D000818:Animals; D017379:Hypertrophy, Left Ventricular / Q000378:metabolism* / Q000473:pathology*; D007375:Interleukin-1 / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology*; D015854:Up-Regulation
D007375:Interleukin-1