Experimental StudiesMyocardial hypertrophy in transgenic mice overexpressing human interleukin 1α*
Section snippets
Construction of IL-1α transgene and generation of TG mice
Construction of the CAG–IL-1α transgene is shown in Fig. 1.
TG mice
Changes were more severe in all tested tissues from 1 of the 2 lines. We report characterization of the founder and F1 offspring from this line. Table 1 shows hIL-1α levels determined by ELISA in 12-day-old TG and WT mice. Values are means ± SD.Empty Cell hIL-1α (pg/mL) Empty Cell TG (n = 6) WT (n = 12) Ventricle 113 ± 32* <4 Atrium 78 ± 19* <4 Lung 50 ± 8* <4 Liver 135 ± 31* <4 Serum 69 ± 12* <4 *P <.01 v WT.
Discussion
In this study we show that constitutively increased levels of hIL-1α in the hearts of TG mice produce cardiomyocyte hypertrophy and heart failure. The developmental overexpression of hIL-1α produced excessive cardiac growth in all TG F1 mice, all of which died before weaning. Northern blotting detected hIL-1α gene expression, and ELISA revealed substantial amounts of hIL-1α protein in TG hearts. Therefore, although we examined only TG F1 mice, we conclude that this cardiac growth response was a
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Reprint requests: Kikuo Isoda, MD, First Department of Medicine, National Defense Medical College, 3-2, Namiki, Tokorozawa, Saitama, 359-0042 Japan.