First Author | Sun JF | Year | 1996 |
Journal | Mouse Genome | Volume | 94 |
Issue | 4 | Pages | 883-4 |
Mgi Jnum | J:38083 | Mgi Id | MGI:85472 |
Citation | Sun JF (1996) The NJS mouse strain: A model of Atherosclerosis. Mouse Genome 94(4):883-4 |
abstractText | Full text of Mouse Genome contribution: THE NJS MOUSE STRAIN: A MODEL OF ATHEROSCLEROSIS. Jing-fang Sun; Medical Animal Experimental Center, Jinling Hospital, Nanjing, P.R. of China. Abstract An inbred mouse strain "NJS" has been bred using continuous brother-sister mating and directional selection for 70-day cholesterol levels on a normal diet. After the 20th generation, the mice were hypercholesterolemic with serum cholesterol levels of 5.65 +/-0.83 mmol/l L-1, a value which is outside the normal range in mice. The incidence of atherosclerosis was 100% in some liable positions such as aortic sac and ascending aorta at 8 months. The most common pathological changes were fatty streaks. Key words: inbred strain, mouse, breeding, characteristics, serum cholesterol, hypercholesterolemia, atherosclerosis, animal model Introduction Atherosclerosis is one of the main causes of death of old people. Its cause has not been fully explored due to lack of good animal models (1, 2). Starting in 1989, the author has developed an inbred strain mouse "NJS" with atherosclerosis. Methods and Results The base population consisted of four pairs of KM outbred mice. During development, the strain has been maintained in barrier breeding unit, and the mice were fed a standard diet with 18% crude protein, 5% fat and 8% water. Mice were selected on 70-day serum cholesterol levels using a standard automatic biochemical analyser. In order to study development of atherosclerosis, mice were killed by an overdose of pentobarbitone at two and eight months of age, the heart was perfused with a 10% formalin, 70% ethanol, and Sudan IV stain in saline in turn. The aorta and the heart were removed and cut open along the smaller bend of the aortic arches and were observed under a 20X dissecting microscope. Sections of the aorta were also examined following standard H and E staining. Serum cholesterol levels from generations seven to 21 are shown in Fig. 1, By the 20th generation the serum cholesterol levels were more than twice as high as those in the base population. No pathological changes were seen at two months of age. However, the incidence of atherosclerosis was 100% at some sites by the age of 8 months. The pathological changes mainly occurred at the edge of the semilunar valve, aortic sac and ascending aorta, with the red-stained lesions having a flaky or stripy appearance (Fig. 2) There was also some staining around the opening of the anonyma arteria, left carotic commonis arteria, left subclavia arteria and arteria intercostales. Most of the changes were fatty streaks. Tissue sections showed many foamy cells in the inner membrane of the ascending aorta. Fibrous and atheromatous plaques were seen in the pulmonalis arteria in female mice (Fig. 3). The strain was typed at 26 biochemical loci, which serve to distinguish it from other strains. It has the H2Kd, H2dk haplotype, and coat colour genes AABBccDD. Breeding performance of the strain is substantially worse than that of the KM base population. Litter size at birth averaged 7.6 +/- 1.6, with 80% survival to weaning. Weaning weight averaged 10.4 +/- 1 g and the 90-day body weight averaged 31.8 +/- 2.1 g in males and 25.5 +/- 1.6 g in females. References: 1) Sun J.F. (1995) Animal models of hypercholesterolemia. Shanghei Laboratory Animal Science 4, 240-242. 2) Sun J.F. and Tian X.Y. (1996) Study on characteristics of inbred NJS mouse strain in atherosclerosis. Chinese Journal of Athersclerosis 4, 162-164. Fig. 1. (Legend). Cholesterol levels in the NJS mouse strain in generations F7-F20. Fig. 2. (Legend). Fatty streaks in aortic sac. Fig. 3. (Legend). Atheromatous plaques. |