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Canstatin modulates L-type calcium channel activity in rat ventricular cardiomyocytes.
Abstract Excessive increase of cytosolic Ca2+ through the activation of L-type Ca2+ channels (LTCCs) via β adrenergic receptor induces apoptosis of cardiomyocytes. Canstatin, a cleaved fragment of collagen type IV α2 chain, is abundantly expressed in normal heart tissue. We previously reported that canstatin inhibits β adrenergic receptor-stimulated apoptosis in cardiomyoblasts. Here, we tested the hyposeis that canstatin regulates LTCCs activity in ventricular cardiomyocytes. Collagen type IV α2 chain (COL4A2) small interfering (si) RNA (for canstatin suppression) or control siRNA was injected via jugular vei...
Source: Biochemical and Biophysical Research communications - April 4, 2018 Category: Biochemistry Authors: Imoto K, Hirakawa M, Okada M, Yamawaki H Tags: Biochem Biophys Res Commun Source Type: research

NOS1AP modulates intracellular Ca(2+) in cardiac myocytes and is up-regulated in dystrophic cardiomyopathy.
Authors: Treuer AV, Gonzalez DR Abstract NOS1AP gene (nitric oxide synthase 1-adaptor protein) is strongly associated with abnormalities in the QT interval of the electrocardiogram and with sudden cardiac death. To determine the role of NOS1AP in the physiology of the cardiac myocyte, we assessed the impact of silencing NOS1AP, using siRNA, on [Ca(2+)]i transients in neonatal cardiomyocytes. In addition, we examined the co-localization of NOS1AP with cardiac ion channels, and finally, evaluated the expression of NOS1AP in a mouse model of dystrophic cardiomyopathy. Using siRNA, NOS1AP levels were reduced to ~30% of...
Source: International Journal of Physiology, Pathophysiology and Pharmacology - November 16, 2014 Category: Physiology Tags: Int J Physiol Pathophysiol Pharmacol Source Type: research