Key result
Tlr2 deficiency significantly enhanced cardiac hypertrophy, demonstrated by a 22.1% higher heart weight to tibia length ratio compared to wild type mice after 14 days of transverse aortic constriction.
Why the study?
Does Tlr2 deficiency prevent the development of left ventricular hypertrophy in a mouse model of transverse aortic constriction induced pressure overload?
Does Tlr2 deficiency prevent the development of left ventricular hypertrophy in a mouse model of transverse aortic constriction induced pressure overload?
Effect estimate: 22.1% higher
p-value: p=<0.01
Genetic disruption of Tlr2 does not prevent, but rather exacerbates, cardiac hypertrophy and ventricular remodeling in a murine model of pressure overload.
Tlr2 deficiency exacerbates TAC-induced hypertrophy in mice; hypothesis-generating and leaves therapeutic role in human LVH open.
BACKGROUND: Toll-like receptors (TLRs) are involved in a variety of cardiovascular disorders, including septic cardiomyopathy, ischemia/reperfusion, heart failure, and cardiac hypertrophy. Previous research revealed that TLR4 promotes cardiac hypertrophy in vivo. Therefore, we investigated whether TLR2 is also involved in the development of cardiac hypertrophy. METHODS: Tlr2 deficient and wild type mice were subjected to transverse aortic constriction (TAC) or sham operation procedure. Left ventricular, heart and lung weights as well as hemodynamic parameters were determined after 3, 14 or 28 days. Real-time RT PCR was used to evaluate left ventricular gene expression. Protein content was determined via ELISA. RESULTS: TAC increased systolic left ventricular pressure, contraction and relaxations velocities as well as the heart weight in both genotypes. Tlr2 deficiency significantly enhanced cardiac hypertrophy after 14 and 28 days of TAC. Left ventricular end-diastolic pressure and heart rate increased in Tlr2(-/-) TAC mice only. Fourteen days of TAC led to a significant elevation of ANP, BNP, TGFβ and TLR4 mRNA levels in Tlr2(-/-) left ventricular tissue. CONCLUSION: These data suggest that Tlr2 deficiency may promote the development of cardiac hypertrophy and ventricular remodeling after transverse aortic constriction.
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Bualeong et al. (2016) studied Cardiac hypertrophy. Tlr2 deficiency (Tlr2-/-) vs. Wild type (Tlr2+/+) was evaluated on Heart weight to tibia length (HW/TL) ratio after 14 days of transverse aortic constriction (22.1% higher, p=<0.01). Tlr2 deficiency significantly enhanced cardiac hypertrophy, demonstrated by a 22.1% higher heart weight to tibia length ratio compared to wild type mice after 14 days of transverse aortic constriction.
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