Differential effects of Pyk2 and FAK on the hypertrophic response of cardiac myocytes.

Menashi EB; Loftus JC

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Differential effects of Pyk2 and FAK on the hypertrophic response of cardiac myocytes.

机译：Pyk2和FAK对心肌细胞肥大反应的差异作用。

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The related cytoplasmic non-receptor tyrosine kinases Pyk2 (proline-rich tyrosine kinase 2) and FAK (focal adhesion kinase) have been implicated in phenylephrine-induced G-protein-coupled receptor-mediated signaling mechanisms leading to cardiomyocyte hypertrophy. We report that, in phenylephrine-stimulated neonatal rat ventricular myocytes (NRVM), Pyk2 augments expression of the hypertrophic marker atrial natriuretic factor (ANF) but reduces cytoskeletal organization and cell spreading. In contrast, FAK attenuates ANF production but does not alter cytoskeletal organization and cell spreading. Pyk2 and FAK exhibit differential localization in both unstimulated and phenylephrine-stimulated myocytes. Pyk2 catalytic activity is required for Pyk2 to augment ANF secretion but is not necessary to reduce cell spreading. Pyk2 autophosphorylation is required but not sufficient for Pyk2 to augment ANF secretion. Expression of the Pyk2 FERM domain as an autonomous fragment inhibits phenylephrine-mediated ANF secretion and reduces cell spreading. In addition, expression of the Pyk2 FERM domain inhibits the ability of Pyk2 to augment ANF secretion; this is correlated with reduced Pyk2 autophosphorylation. These data indicate that Pyk2 and FAK have different roles and occupy different positions in signaling pathways leading to the development of cardiomyocyte hypertrophy.

机译：相关的细胞质非受体酪氨酸激酶Pyk2（富含脯氨酸的酪氨酸激酶2）和FAK（局灶性粘附激酶）与去氧肾上腺素诱导的G蛋白偶联受体介导的信号传导机制有关，导致心肌肥大。我们报告，在去氧肾上腺素刺激的新生大鼠心室肌细胞（NRVM）中，Pyk2增强了肥厚性标志性心钠素（ANF）的表达，但减少了细胞骨架组织和细胞扩散。相反，FAK会减弱ANF的产生，但不会改变细胞骨架的组织和细胞扩散。 Pyk2和FAK在未刺激和去氧肾上腺素刺激的心肌细胞中均表现出不同的定位。 Pyk2增加ANF分泌需要Pyk2催化活性，但减少细胞散布不是必需的。 Pyk2自磷酸化是必需的，但不足以使Pyk2增强ANF分泌。 Pyk2 FERM域作为自主片段的表达抑制了去氧肾上腺素介导的ANF分泌并减少了细胞扩散。另外，Pyk2 FERM结构域的表达抑制了Pyk2增强ANF分泌的能力。这与减少的Pyk2自磷酸化有关。这些数据表明Pyk2和FAK具有不同的作用，并在导致心肌肥大发展的信号传导途径中占据不同的位置。

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《Cell and Tissue Research》 |2009年第2期|共13页
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Menashi EB; Loftus JC;
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1. Differential effects of Pyk2 and FAK on the hypertrophic response of cardiac myocytes. [J] . Menashi EB, Loftus JC Cell and Tissue Research . 2009,第2期

机译：Pyk2和FAK对心肌细胞肥大反应的差异作用。
2. Disruption of the cyclic AMP phosphodiesterase-4 (PDE4)-HSP20 complex attenuates the beta-agonist induced hypertrophic response in cardiac myocytes. [J] . Sin YY, Edwards HV, Li X, Journal of Molecular and Cellular Cardiology . 2011,第5期

机译：环状AMP磷酸二酯酶4（PDE4）-HSP20复合物的破坏减弱了β-激动剂诱导的心肌细胞肥大反应。
3. Chronic activation of extracellular-signal-regulated protein kinases by phenylephrine is required to elicit a hypertrophic response in cardiac myocytes. [J] . Barron AJ, Finn SG, Fuller SJ The Biochemical Journal . 2003,第Pta1期

机译：需要去氧肾上腺素对细胞外信号调节的蛋白激酶进行长期激活，以引起心肌细胞的肥大反应。
4. Modeling Cardiac Hemodynamic Response During Exercise in Health and Hypertrophic Cardiomyopathy [C] . I. Farro, C. R. Arbeitman, L. J. Cymberknop, Annual International Conference of the IEEE Engineering in Medicine and Biology Society . 2018

机译：在健康和肥厚性心肌病运动过程中模拟心脏血液动力学反应
5. The Contributions of FAK and Pyk2 to Osteoclast Function and Bone Homeostasis [D] . Ray, Brianne Jeriel 2011

机译：FAK和Pyk2对破骨细胞功能和骨稳态的贡献
6. Differential effects of Pyk2 and FAK on the hypertrophic response of cardiac myocytes [O] . Emmanuel B. Menashi, Joseph C. Loftus -1

机译：PYK2和FAK对心肌细胞肥厚响应的差异影响
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Differential effects of Pyk2 and FAK on the hypertrophic response of cardiac myocytes.

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