Changes in electrophysiological properties, such as ion channel expression and activity,
are closely related to arrhythmogenesis during heart failure (HF). However, a causative
factor for the electrical remodeling in HF has not been determined. Periostin (POSTN), a
matricellular protein, is increased in heart tissues of patients with HF. In the present
study, we investigated whether a single injection of POSTN affects the
electrophysiological properties in rat ventricles. After male Wistar rats were
intravenously injected with recombinant rat POSTN (64 µg/kg, 24 hr), electrocardiogram
(ECG) was recorded. Whole-cell patch clamp was performed to measure action potential (AP)
and Na
+
current (
I
Na
) in isolated ventricular
myocytes. Protein expression of cardiac voltage-gated Na
+
channel
(Na
V
1.5) in isolated ventricles was examined by Western blotting. In ECG,
POSTN-injection significantly increased RS height. POSTN-injection significantly delayed
time to peak in AP and decreased
I
Na
in the isolated
ventricular myocytes. POSTN-injection decreased Na
V
1.5 expression in the
isolated ventricles. It was confirmed that POSTN (1 µg/ml, 24 hr) decreased
I
Na
and Na
V
1.5 protein expression in neonatal rat
ventricular myocytes. This study for the first time demonstrated that a single injection
of POSTN in rats decreased
I
Na
by suppressing
Na
V
1.5 expression in the ventricular myocytes, which was accompanied by a
prolongation of time to peak in AP and an increase of RS height in ECG.
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