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首页> 外文期刊>American Journal of Physiology >Role of protein kinase C-epsilon in hypertrophy of cultured neonatal rat ventricular myocytes.
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Role of protein kinase C-epsilon in hypertrophy of cultured neonatal rat ventricular myocytes.

机译：蛋白激酶C-ε在培养的新生大鼠心室肌细胞肥大中的作用。

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摘要

Using adenovirus (Adv)-mediated overexpression of constitutively active (ca) and dominant-negative (dn) mutants, we examined whether protein kinase C (PKC)-epsilon, the major novel PKC isoenzyme expressed in the adult heart, was necessary and/or sufficient to induce specific aspects of the hypertrophic phenotype in low-density, neonatal rat ventricular myocytes (NRVM) in serum-free culture. Adv-caPKC-epsilon did not increase cell surface area or the total protein-to-DNA ratio. However, cell shape was markedly affected, as evidenced by a 67% increase in the cell length-to-width ratio and a 17% increase in the perimeter-to-area ratio. Adv-caPKC-epsilon also increased atrial natriuretic factor (ANF) and beta-myosin heavy chain (MHC) mRNA levels 2.5 +/- 0.3- and 2.1 +/- 0.2-fold, respectively, compared with NRVM infected with an empty, parent vector (P < 0.05 for both). Conversely, Adv-dnPKC-epsilon did not block endothelin-induced increases in cell surface area, the total protein-to-DNA ratio, or upregulation of beta-MHC and ANF gene expression. However, the dominant-negative inhibitor markedly suppressed endothelin-induced extracellular signal-regulated kinase (ERK) 1/2 activation. Taken together, these results indicate that caPKC-epsilon overexpression alters cell geometry, producing cellular elongation and remodeling without a significant, overall increase in cell surface area or total protein accumulation. Furthermore, PKC-epsilon activation and downstream signaling via the ERK cascade may not be necessary for cell growth, protein accumulation, and gene expression changes induced by endothelin.
机译：使用腺病毒（Adv）介导的组成性活性（ca）和显性负性（dn）突变体的过表达，我们检查了成年心脏中表达的主要新型PKC同工酶蛋白激酶C（PKC）-ε是否必要和/或或足以在无血清培养的低密度新生大鼠心室肌细胞（NRVM）中诱导肥大表型的特定方面。 Adv-caPKC-epsilon不会增加细胞表面积或总蛋白与DNA的比率。但是，细胞形状受到显着影响，细胞长宽比增加了67％，周长比增加了17％，证明了这一点。与感染空父母的NRVM相比，Adv-caPKC-epsilon还分别增加了房性利钠因子（ANF）和β-肌球蛋白重链（MHC）mRNA水平2.5 +/- 0.3-倍和2.1 +/- 0.2倍。向量（两者均P <0.05）。相反，Adv-dnPKC-ε并不能阻止内皮素诱导的细胞表面积，总蛋白质与DNA比率的增加或β-MHC和ANF基因表达的上调。但是，显性负抑制剂显着抑制了内皮素诱导的细胞外信号调节激酶（ERK）1/2活化。综上所述，这些结果表明，caPKC-ε的过表达改变了细胞的几何形状，产生了细胞的伸长和重塑，而细胞表面积或总蛋白的积累却没有明显的整体增加。此外，PKC-ε激活和通过ERK级联的下游信号传导可能不是内皮素诱导的细胞生长，蛋白质积累和基因表达变化的必要条件。

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