RAGE upregulation and nuclear factor-κB activation associated with ageing rat cardiomyocyte dysfunction

Rok, strany: 2008, 152 - 158

Evidence suggests that ageing is a major risk factor for cardiac dysfunction. Interactions between advanced glycation endproducts (AGEs) and the receptor for AGEs (RAGE) are known to cause chronic cellular activation, including activation of nuclear factor-κB (NF-κB), which has been implicated as a causal factor in the ageing process. To assess whether cardiomyocyte contractile function and the interaction of AGEs with RAGE in the heart are altered in ageing, 25- and 2-month-old male rats were compared. Mechanical properties were assessed in ventricular myocytes using an edge-detection system, including peak twitch amplitude (PTA), time-to-PTA (TPS), time-to-75% relengthening (TR75) and maximal velocity of shortening/relengthening (±dL/dt) in ventricular myocytes. AGEs were detected by using a fluorescence assay. The expression of RAGE and NF-κB was assessed through a Western blot analysis. Compared with young myocytes, aged myocytes displayed a prolonged TR75 at 1 Hz. With increasing stimulus frequency (from 2 to 4 Hz), aged myocytes' PTA was significantly reduced relative to young myocytes. Aged rat hearts displayed high level of AGEs, RAGE upregulation and NF-κB activation. These findings demonstrate impaired cardiomyocyte relaxation and reduced tolerance to increased stimulus frequency in aged rats, which might be associated with enhanced AGEs, RAGE expression, and NF-κB activation.

ISO 690:

Gao, Z., Yang, C., Wang, Y., Wang, P., Chen, H., Zhang, X., Liu, R., Li, W., Qin, X., Liang, X., Hai, C. 2008. RAGE upregulation and nuclear factor-κB activation associated with ageing rat cardiomyocyte dysfunction. In General Physiology and Biophysics, vol. 27, no.3, pp. 152-158. 0231-5882.

APA:

Gao, Z., Yang, C., Wang, Y., Wang, P., Chen, H., Zhang, X., Liu, R., Li, W., Qin, X., Liang, X., Hai, C. (2008). RAGE upregulation and nuclear factor-κB activation associated with ageing rat cardiomyocyte dysfunction. General Physiology and Biophysics, 27(3), 152-158. 0231-5882.