Interaction of genetic background and exercise training intensity on endothelial function in mouse aorta

The purpose of this study was to characterize the genetic contribution to endothelial adaptation to exercise training. Vasoreactivity was assessed in aortas from four inbred mouse strains (129S1, B6, NON, and SJL) after 4 weeks of moderate intensity continuous exercise training (MOD), high intensity interval training (HIT) or in sedentary controls (SED). Intrinsic variations in endothelium-dependent vasorelaxation (EDR) to acetylcholine (ACh) as well as vasocontractile responses were observed across SED groups. For responses to exercise training, there was a significant interaction between mouse strain and training intensity on EDR. Exercise training had no effect on EDR in aortas from 129S1 and B6 mice. In NON, EDR was improved in aortas from MOD and HIT compared with respective SED, accompanied by diminished responses to PE in those groups. Interestingly, EDR was impaired in aorta from SJL HIT compared with SED. The transcriptional activation of endothelial genes was also influenced by the interaction between mouse strain and training intensity. The number of genes altered by HIT was greater than MOD, and there was little overlap between genes altered by HIT and MOD. HIT was associated with gene pathways for inflammatory responses. NON MOD genes showed enrichment for vessel growth pathways. These findings indicate that exercise training has non-uniform effects on endothelial function and transcriptional activation of endothelial genes depending on the interaction between genetic background and training intensity.

Distortion Product Otoacoustic Emissions in Age-related Hearing Loss of C57 and BALB/c Inbred Mouse Strains / 听力学及言语疾病杂志

Objective To assess the dynamic age-related hearing loss of inbred mouse C57 and BALB/c strains via distortion product otoacoustic emissions(DPOAE). Methods DPOAE levels were evaluated in C57 and BALB/c of 20,30,60,90,120,150,180 days old respectively,with the conditions that two pure tones,which stimulated the DPOAE,were at frequencies(f 1,f 2,f 1/f 2=1.22)and levels(L 1=70 dB SPL,L 2=65 dB SPL).Results DPOAE levels of C57 and BALB/c gradually decreased with age.From 60 days old,DPOAE levels of the two strains were dramatically decreased at 4.0,6.0,8.0 kHz( P

The study of bone atrophy on the tail-up suspension in the inbred strain mice / 体力科学

A study was conducted to investigate the mechanism of bone atrophy in various strains of inbred mice under the influence of tail-up suspension. Nine inbred strains of mice (NZB/N, NZW/N, AKR/N, Balb/C, C 57 BL, C 3 H/He, A/J, DBA, CBA/N) aged six weeks were used. Each strain was divided randomly into two groups, a suspension group (SG; n=5) and a control group (CG; n=5) . The suspension group were etherized and suspended with an elastic bandage. After one week, the tibiae were removed and their bone weights were measured using an electric balance (Metler; AE 240) . Their length was also measured with a vernier caliper. In all strains, body weight in the SG was significantly lower than that in the CG. From the bone weight and length in the CG, bone growth in the NZB/N, AKR/N, NZW/N and C3H/He strains was considered to be higher than in the other strains. On the other hand bone growth in the DBA, A/J, Balb/C, and CBA/N strains were lower than in the others. The absolute value of bone weight in the SG was significantly smaller than that in the CG in six strains (NZB/N, C 57 BL, A/J, NZW/N, C 3 H/He, Balb/C) . However in the DBA strain, the absolute value of bone weight in the SG was significantly higher than that in the CG.<BR>From the results of this investigation we suggest that the mechanism of normal bone growth is not the same as the mechanism of bone atrophy induced by tail-up suspension.