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首页> 外文期刊>Journal of Cellular Physiology >Strain activation of bovine aortic smooth muscle cell proliferation and alignment: study of strain dependency and the role of protein kinase A and C signaling pathways.
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Strain activation of bovine aortic smooth muscle cell proliferation and alignment: study of strain dependency and the role of protein kinase A and C signaling pathways.

机译：牛主动脉平滑肌的应变激活细胞增殖和对齐:研究应变依赖和蛋白激酶A和C的作用信号通路。

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Smooth muscle cell (SMC) phenotype can be altered by physical forces as demonstrated by cyclic strain-induced changes in proliferation, orientation, and secretion of macromolecules. However, the magnitude of strain required and the intracellular coupling pathways remain ill defined. To examine the strain requirements for SMC proliferation, we selectively seeded bovine aortic SMC either on the center or periphery of silastic membranes which were deformed with 150 mm Hg vacuum (0-7% center; 7-24% periphery). SMC located in either the center or peripheral regions showed enhanced proliferation compared to cells grown under the absence of cyclic strain. Moreover, SMC located in the center region demonstrated significantly (P < 0.005) greater proliferation as compared to those in the periphery. In contrast, SMC exposed to high strain (7-24%) demonstrated alignment perpendicular to the strain gradient, whereas SMC in the center (0-7%) remained aligned randomly. To determine the mechanisms of these phenomena, we examined the effect of cyclic strain on bovine aortic SMC signaling pathways. We observed strain-induced stimulation of the cyclic AMP pathway including adenylate cyclase activity and cyclic AMP accumulation. In addition, exposure of SMC to cyclic strain caused a significant increase in protein kinase C (PKC) activity and enzyme translocation from the cytosol to a particulate fraction. Further study was conducted to examine the effect of strain magnitude on signaling, particularly protein kinase A (PKA) activity as well as cAMP response element (CRE) binding protein levels. We observed significantly (P < 0.05) greater PKA activity and CRE binding protein levels in SMC located in the center as compared to the peripheral region. However, inhibition of PKA (with 10 microM Rp-cAMP) or PKC (with 5-20 ng/ml staurosporine) failed to alter either the strain-induced increase in SMC proliferation or alignment. These data characterize the strain determinants for activation of SMC proliferation and alignment. Althoughstrain activated both the AC/cAMP/PKA and the PKC pathways in SMC, singular inhibition of PKA and PKC failed to prevent strain-induced alignment and proliferation, suggesting either their lack of involvement or the multifactorial nature of these responses.
机译：平滑肌细胞(SMC)表型是可以改变的由物理部队,证明了循环应变变化的扩散,定位、和大分子的分泌。然而,应变的大小和要求细胞内的耦合途径仍然是生病定义的。SMC增殖,我们选择性地播种牛主动脉SMC的中心或边缘与150年硅橡胶膜的变形毫米汞柱真空(0 - 7%的中心;位于中心或外围区域显示增强扩散相比细胞生长的缺席下循环应变。此外,SMC位于中心地区显示出了明显(P < 0.005)相比那些增殖外围。应变(7 - 24%)显示对齐垂直于应变梯度,而SMC在中心随机(0 - 7%)保持一致。确定这些现象的机制,我们在牛检查循环应变的影响主动脉SMC信号通路。应变环腺苷酸的刺激包括腺苷酸环化酶活性和途径环腺苷酸积累。SMC循环造成很大压力蛋白激酶C (PKC)活性和增加从胞质酶易位颗粒分数。检查压力大小的影响信号,尤其是蛋白激酶A (PKA)营活动以及响应元件(CRE)结合蛋白的水平。(P < 0.05)更大的PKA活性和CRE绑定蛋白质含量在SMC位于中心与周边地区相比。抑制PKA (10 microM Rp-cAMP)或PKC(5 - 20 ng / ml staurosporine)未能改变SMC的应变增长增殖或对齐。描述应变的决定因素激活SMC增殖和对齐。Althoughstrain AC /营地/ PKA和激活SMC的PKC途径,单一的抑制PKA和PKC未能阻止应变校准和扩散,暗示他们缺乏或多因子的参与这些反应的性质。

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