Key result
Urotensin II dose-dependently induces hypertrophy and ANP/BNP expression in cultured rat cardiomyocytes.
Why the study?
The role of urotensin II in regulating hypertrophy in cardiomyocytes was not well understood.
Does Urotensin II induce hypertrophic responses in cultured cardiomyocytes from neonatal rats?
Does Urotensin II induce hypertrophic responses in cultured cardiomyocytes from neonatal rats?
Urotensin II induces hypertrophic responses in cultured neonatal rat cardiomyocytes, suggesting a potential role in the development of cardiac hypertrophy.
May implicate urotensin II in cardiomyocyte hypertrophy; hypothesis-generating and requires in vivo and human validation.
Urotensin II (UII), a cyclic neuropeptide, functions not only in the central nervous system but also in non-neural systems including cardiovascular systems. In the present study we examined whether UII regulates hypertrophy in cardiomyocytes. The exposure of cultured cardiomyocytes from neonatal rats to UII dose-dependently activated extracellular signal-regulated kinases (ERKs), important molecules in the development of cardiac hypertrophy. ERK activation by UII at 100 nM peaked at 8 min after stimulation. UII markedly induced expression of specific genes encoding atrial natriuretic peptide and brain natriuretic peptide, and significantly increased amino acid incorporation into proteins. Incubation of cardiomyocytes with UII increased cell size and myofibril organisation. UII, then, might participate in cardiomyocyte hypertrophy.
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Zou et al. (2001) studied Cardiac hypertrophy. Urotensin II (UII) was evaluated on Hypertrophic responses including ERK activation, gene expression of ANP and BNP, amino acid incorporation, cell size, and myofibril organisation. Exposure of cultured neonatal rat cardiomyocytes to Urotensin II dose-dependently activated ERKs, induced ANP and BNP gene expression, and increased cell size and myofibril organisation.
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