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van der Pouw Kraan, T.C., Bernink, F.J., Yildirim, C., Koolwijk, P., Baggen, J.M., Timmers, L., Beek, A.M., Diamant, M., Chen, W.J., van Rossum, A.C., van Royen, N., Horrevoets, A.J. and Appelman, Y.E. (2014) Systemic Toll-Like Receptor and Interleukin-18 Pathway Activation in Patients with Acute ST Elevation Myocardial Infarction. Journal of Molecular and Cellular Cardiology, 67, 94-102.
https://doi.org/10.1016/j.yjmcc.2013.12.021
has been cited by the following article:
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TITLE:
Forskolin Modulates the Inhibitory Effect of C-Type Natriuretic Peptide on Hypoxia-Induced Atrial Dynamics and Hypoxia Inducible Factor 1 Alpha Activity
AUTHORS:
Chengming Guan, Yanan Jia, Chaochao Bian, Bo Zhang, Dazhi Ding, Xun Cui
KEYWORDS:
C-Type Natriuretic Peptide, Hypoxia Inducible Factor-1α, Phosphodiesterase, Adenylyl Cyclase, Forskolin
JOURNAL NAME:
Journal of Biosciences and Medicines,
Vol.5 No.1,
January
3,
2017
ABSTRACT: Our study investigated effects of C-type natriuretic peptide (CNP) on atrial dynamics and hypoxia inducible factor 1 alpha (HIF-1α) activity in perfused beating rat atria, under hypoxic conditions. Hypoxia significantly increased the levels of HIF-1α, concomitant with decreased trial dynamics. CNP (0.1 μmol/L) further decreased atrial dynamics under hypoxia and suppressed hypoxia-induced stimulation of HIF-1α expression. An adenylylcyclase (AC) activator, forskolin (0.1 μmol/L), significantly up-regulated atrial phosphodiesterase subtype 3A (PDE 3A) protein without affecting hypoxia-induced dynamics. In the presence of forskolin, the inhibitory effects of CNP on hypoxia-induced atrial dynamics and HIF-1α levels were significantly attenuated. Forskolin also prevented hypoxia-induced downregulation of PDE3A protein. These findings suggested that CNP inhibited atrial dynamics and HIF-1α activity in the isolated perfused beating rat atria under hypoxic conditions. Furthermore, both effects were modulated by the AC activator forskolin, through activation of CNP-PDE 3A signaling.