Department of Physics, Friedrich-Alexander-University of Erlangen-Nuremberg, Erlangen, Germany.
Biochem Biophys Res Commun. 2011 Oct 7;413(4):541-4. doi: 10.1016/j.bbrc.2011.08.133. Epub 2011 Sep 6.
Mechano-transduction was studied in wildtype and focal adhesion (FA) protein-deficient mouse embryonic fibroblasts (MEFs). Using a cell stretcher, we determined the effect of stretch on cell morphology, apoptosis, and phosphorylation of ERK(1/2). After 20% cyclic, uniaxial stretch, FA-deficient MEFs showed morphological changes and levels of apoptosis of the order: focal adhesion kinase>p130Cas>vinculin compared to wildtype cells. ERK(1/2) phosphorylation peaked in wildtype cells at around 10 min, and in all FA-deficient cells at around 5 min. The relative change in strain energy of FA-deficient cells compared to wildtype cells was of the order: vinculin>FAK>p130Cas. Taken together, FAK and p130Cas are more important in the stretch-mediated downstream signaling and cell survival pathway, while vinculin is more critical in maintaining cell contractility.
机械转导在野生型和黏着斑（FA）蛋白缺陷型鼠胚胎成纤维细胞（MEFs）中进行了研究。使用细胞拉伸器，我们确定了拉伸对细胞形态、细胞凋亡和 ERK(1/2)磷酸化的影响。在 20%的循环、单轴拉伸后，FA 缺陷型 MEFs 表现出形态变化和凋亡水平，其顺序为：黏着斑激酶 > p130Cas > 整联蛋白，与野生型细胞相比。ERK(1/2)磷酸化在野生型细胞中于约 10 分钟达到峰值，而在所有 FA 缺陷型细胞中于约 5 分钟达到峰值。FA 缺陷型细胞与野生型细胞的应变能相对变化顺序为：整联蛋白 > FAK > p130Cas。总之，FAK 和 p130Cas 在拉伸介导的下游信号和细胞存活途径中更为重要，而整联蛋白在维持细胞收缩性方面更为关键。
