Key result
The selective ROCK inhibitor Y27632 inhibited ET-1-induced increases in natriuretic peptide production, cell size, protein synthesis, and myofibrillar organization in neonatal rat cardiac myocytes.
Why the study?
Does ROCK inhibition with Y27632 prevent ET-1-induced hypertrophic responses in neonatal rat cardiac myocytes?
Does ROCK inhibition with Y27632 prevent ET-1-induced hypertrophic responses in neonatal rat cardiac myocytes?
The Rho/ROCK pathway is an important component of ET-1-induced hypertrophic signals in cardiac myocytes, suggesting ROCK inhibition as a potential mechanism to prevent cardiac hypertrophy.
Answers are grounded in this paper and cite their sources.
May support ROCK inhibition in hypertrophy; hypothesis-generating for clinical translation.
A small GTPase, Rho, participates in agonist-induced cytoskeletal organization and gene expression in many cell types including cardiac myocytes. However, little is known about the functions of Rho's downstream targets in cardiac myocytes. We examined the role of ROCK, a downstream target of Rho, in ET-1-induced hypertrophic response. Y27632, a selective ROCK inhibitor, inhibited ET-1-induced increases in natriuretic peptide production, cell size, protein synthesis, and myofibrillar organization. In addition, a dominant-negative mutant of p160ROCK suppressed ET-1-induced transcription of the BNP gene. These findings suggest that the Rho/ROCK pathway is an important component of ET-1-induced hypertrophic signals in cardiac myocytes.
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Kuwahara et al. (1999) studied ET-1-induced hypertrophic response in neonatal rat cardiac myocytes. Y27632 was evaluated on ET-1-induced increases in natriuretic peptide production, cell size, protein synthesis, and myofibrillar organization. The selective ROCK inhibitor Y27632 inhibited ET-1-induced increases in natriuretic peptide production, cell size, protein synthesis, and myofibrillar organization in neonatal rat cardiac myocytes.
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