Home General Physiology and Biophysics 2008 General Physiology and Biophysics Vol.27, p.152-158, 2008

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Quarterly, 80 pp. per issue
Founded: 1982
ISSN  1338-4325 (online)

Published in English

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General Physiology and Biophysics Vol.27, p.152-158, 2008

Title: RAGE upregulation and nuclear factor-κB activation associated with ageing rat cardiomyocyte dysfunction
Author: Z. Q. Gao, C. Yang, Y. Y. Wang, P. Wang, H. L. Chen, X. D. Zhang, R. Liu, W. L. Li, X. J. Qin, X. Liang, Ch. X. Hai

Abstract: 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.

Keywords: Cardiac myocytes — Ageing — Advanced glycation endproducts — Receptor for AGEs — Nuclear factor-κB
Year: 2008, Volume: 27, Issue: Page From: 152, Page To: 158

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