Key result
Overexpression of constitutively active PKC-epsilon in neonatal rat ventricular myocytes altered cell geometry and increased ANF and beta-MHC mRNA levels (P<0.05) without increasing cell surface area.
p-value: p=<0.05
PKC-epsilon activation induces cellular elongation and specific gene expression changes but is not necessary for endothelin-induced overall cell growth in neonatal rat ventricular myocytes.
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PKC-epsilon drives myocyte elongation and gene expression without growth in vitro; leaves open its necessity in cardiac hypertrophy and requires in vivo validation.
Strait et al. (2001) studied Hypertrophy (in vitro model). Adenovirus-mediated overexpression of constitutively active (ca) and dominant-negative (dn) PKC-epsilon mutants vs. Empty parent vector or endothelin was evaluated on Cell surface area, total protein-to-DNA ratio, cell shape, and gene expression (ANF, beta-MHC) (p=<0.05). Overexpression of constitutively active PKC-epsilon in neonatal rat ventricular myocytes altered cell geometry and increased ANF and beta-MHC mRNA levels (P<0.05) without increasing cell surface area.
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