Abstract
Objectives: Many studies indicate the involvement of transient receptor potential (TRP) channels in the development of heart hypertrophy. However, the data is often conflicted and has originated in animal models. Here, we provide systematic analysis of TRP channels expression in human failing myocardium. Methods and results: Left-ventricular tissue samples were isolated from explanted hearts of NYHA III-IV patients undergoing heart transplants (n = 43). Quantitative real-time PCR was performed to assess the mRNA levels of TRPC, TRPM and TRPV channels. Analysis of functional, clinical and biochemical data was used to confirm an end-stage heart failure diagnosis. Compared to myocardium samples from healthy donor hearts (n = 5), we detected a distinct increase in the expression of TRPC1, TRPC5, TRPM4 and TRPM7, and decreased expression of TRPC4 and TRPV2. These changes were not dependent on gender, clinical or biochemical parameters, nor functional parameters of the heart. We detected, however, a significant correlation of TRPC1 and MEF2c expression. Conclusions: The end-stage heart failure displays distinct expressional changes of TRP channels. Our findings provide a systematic description of TRP channel expression in human heart failure. The results highlight the complex interplay between TRP channels and the need for deeper analysis of early stages of hypertrophy and heart failure development.
Highlights
Heart failure (HF) is a culmination of different pathophysiological conditions on heart muscle which cause progressive worsening of heart function [1]
The diagnosed HF was in last stages as shown by the left ventricle ejection fraction (LVEF) that was decreased to 22.64 ± 1.407%
The expression of TRPM2 channel was not altered in HF, we detected significantly increased expression of TRPM4 and TRPM7 channels
Summary
Heart failure (HF) is a culmination of different pathophysiological conditions on heart muscle which cause progressive worsening of heart function [1]. HF is preceded by impaired calcium homeostasis—Contraction and Ca2+ transients are markedly prolonged and restoration of low diastolic Ca2+ concentrations is impaired [4]. Increased Ca2+ levels during diastole can be related to depressed protein expression levels of sarco/endoplasmic reticulum Ca2+ -ATPase (SERCA) or decreased rates of sarcoplasmic reticulum (SR) Ca2+ uptake [5]. After depletion of internal Ca2+ stores, the store-operated calcium entry (SOCE) is activated [6]. Multiple proteins and channels are involved in SOCE, e.g., STIM proteins, Orai channels or channels from the transient receptor potential (TRP) family
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