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首页> 外文学位 >Expression and regulation of protein kinase C (PKC) isozymes in neonatal rat cardiac myocytes.
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Expression and regulation of protein kinase C (PKC) isozymes in neonatal rat cardiac myocytes.

机译：蛋白激酶C（PKC）同工酶在新生大鼠心肌细胞中的表达和调控。

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摘要

Altered PKC expression has been associated with animal models of pressure-overload induced hypertrophy, MI, reperfusion injury, aortic stenosis and heart failure. The goals of this work were to determine whether angiotensin II (Ang II), the extracellular matrix (ECM) or mechanical stretch alter PKC isozyme expression.; Application of Ang II to neonatal rat myocyte cultures resulted in the translocation of PKC alpha from the particulate fraction to the cytoplasmic fraction. Application of Ang II failed to have an effect on PKC delta, epsilon or zeta. Blockade of the Ang II type 1 receptor with Losartan inhibited the translocation while, the Ang II type 2 receptor PD 123,319 had no effect, suggesting that PKC alpha is involved in Ang II signaling via the AT1R.; We examined the role of PKC isozymes in attachment, cell volume and myofibril formation on different ECM substrates by utilizing PKC inhibitors. Rottlerin, inhibited attachment to laminin, fibronectin, collagen and aligned collagen in a dose dependent manner, decreased cell volume on laminin and collagen and inhibited myofibril formation on laminin. Go 6976 inhibited attachment to collagen, and Bisindolylmaleimide I decreased cell volume on laminin. It appears that PKCs and/or their down stream effectors play an important role in the interaction between cardiac myocytes and their surrounding matrix.; We utilized a 3-dimensional culture system examine how the intensity, direction and nature (cyclic vs. static) of stretch affects the expression of PKC alpha, delta, and epsilon. Cyclic and static stretch perpendicular to myocyte alignment increased PKC delta. PKC epsilon expression increased following cyclic stretch perpendicular to myocyte alignment. PKC alpha expression was not altered by the type, direction, or intensity of stretch. These results indicate that PKC delta and epsilon may be one mechanism for cardiac myocytes to discriminate between different directions and intensities of mechanical stretch. In conclusion, these experiments demonstrate that PKC isozyme expression is altered by Ang II, ECM composition and mechanical stretch.
机译：PKC表达改变与压力超负荷引起的肥大，心肌梗死，再灌注损伤，主动脉瓣狭窄和心力衰竭的动物模型有关。这项工作的目的是确定血管紧张素II（Ang II），细胞外基质（ECM）或机械拉伸是否改变PKC同工酶的表达。 Ang II在新生大鼠心肌细胞培养物中的应用导致PKCα从颗粒级分转移到细胞质级分。 Ang II的使用对PKCδ，ε或zeta无效。用洛沙坦对Ang II 1型受体的阻断抑制了易位，而Ang II 2型受体PD 123,319没有作用，表明PKC alpha通过AT1R参与了Ang II信号传导。我们通过利用PKC抑制剂研究了PKC同工酶在不同ECM底物上的附着，细胞体积和肌原纤维形成中的作用。 Rottlerin以剂量依赖性方式抑制层粘连蛋白，纤连蛋白，胶原蛋白和对齐的胶原蛋白的附着，减少层粘连蛋白和胶原蛋白的细胞体积，并抑制层粘连蛋白的肌原纤维形成。 Go 6976抑制了对胶原的附着，而Bisindolylmaleimide I减少了层粘连蛋白上的细胞体积。似乎PKC和/或其下游效应子在心肌细胞与其周围基质之间的相互作用中起重要作用。我们利用3维培养系统检查拉伸的强度，方向和性质（循环与静态）如何影响PKCα，δ和ε的表达。垂直于心肌细胞排列的循环和静态拉伸增加了PKC增量。垂直于心肌细胞排列的周期性拉伸后，PKC epsilon表达增加。 PKCα的表达没有被拉伸的类型，方向或强度改变。这些结果表明PKCδ和ε可能是心肌细胞区分机械拉伸不同方向和强度的一种机制。总之，这些实验表明，PKC同工酶表达被Ang II，ECM组成和机械拉伸改变。

著录项

  • 作者

    Bullard, Tara Anne.;

  • 作者单位

    University of South Carolina.;

  • 授予单位 University of South Carolina.;
  • 学科 Biology Anatomy.; Biology Cell.
  • 学位 Ph.D.
  • 年度 2004
  • 页码 216 p.
  • 总页数 216
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 生物形态学;细胞生物学;
  • 关键词

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