Biochemical and Cellular Determinants of Renal Glomerular Elasticity.
Biochemical and Cellular Determinants of Renal Glomerular Elasticity.
复制标题
DOI：
10.1371/journal.pone.0167924
复制
发表时间：
2016
期刊：
影响因子：
3.7
通讯作者：
Miller RT
中科院分区：
文献类型：
--
作者：
Embry AE;Mohammadi H;Niu X;Liu L;Moe B;Miller-Little WA;Lu CY;Bruggeman LA;McCulloch CA;Janmey PA;Miller RT
肾小球及其毛细血管的弹性特性使它们能够在不同的血流动力作用下保持结构的完整性。通过微压痕测量，肾小球的弹性系数(E，Young‘s)为2.1kPa.根据肾小球血流灌注研究的估计，肾小球的弹性系数介于2至4kpa之间。由Latrunculin解聚的F-肌动蛋白、由Blebbistatin抑制的Acto-myosin收缩、减少ATP合成以及由EDTA降低黏附蛋白的亲和力使肾小球E分别降至1.26、1.7、1.5和1.43 kpa。用茉莉花内酯稳定肌动蛋白细丝和增加整合素与镁离子的亲和力分别使E增加到2.65和2.87 kPa.肾小球E的改变反映在F/G肌动蛋白比率的相应变化上。With aferin A破坏Vimentin中间丝使E降至0.92kPa.脱细胞肾小球的弹性系数为0.74kPa.说明肾小球的细胞成分对其弹性有主导作用。磁珠位移法测得肾小球基底膜的E为2.4kPa.在E值为3~5kPa的基质上生长的足细胞和系膜细胞具有肌动蛋白纤维和类似于体内足细胞的局灶性粘连。肾缺血和缺血再灌流使肾小球E降至1.58kPa.这些结果表明，肾小球的E在2~4kpa之间。2.4kPaGBM的E值与此值一致，并受到生长在可变刚度矩阵上的足细胞和系膜细胞行为的支持。足细胞骨架是肾小球E的主要组成部分，正常的E需要ATP的合成。缺血和其他疾病后肾小球E的减少表明，肾小球E的减少是许多形式的肾小球损伤的共同特征，并提示足细胞细胞骨架异常。
The elastic properties of renal glomeruli and their capillaries permit them to maintain structural integrity in the presence of variable hemodynamic forces. Measured by micro-indentation, glomeruli have an elastic modulus (E, Young’s modulus) of 2.1 kPa, and estimates from glomerular perfusion studies suggest that the E of glomeruli is between 2 and 4 kPa. F-actin depolymerization by latrunculin, inhibition of acto-myosin contractility by blebbistatin, reduction in ATP synthesis, and reduction of the affinity of adhesion proteins by EDTA reduced the glomerular E to 1.26, 1.7, 1.5, and 1.43 kPa, respectively. Actin filament stabilization with jasplakinolide and increasing integrin affinity with Mg2+ increased E to 2.65 and 2.87 kPa, respectively. Alterations in glomerular E are reflected in commensurate changes in F/G actin ratios. Disruption of vimentin intermediate filaments by withaferin A reduced E to 0.92 kPa. The E of decellularized glomeruli was 0.74 kPa, indicating that cellular components of glomeruli have dominant effects on their elasticity. The E of glomerular basement membranes measured by magnetic bead displacement was 2.4 kPa. Podocytes and mesangial cells grown on substrates with E values between 3 and 5 kPa had actin fibers and focal adhesions resembling those of podocytes in vivo. Renal ischemia and ischemia-reperfusion reduced the E of glomeruli to 1.58 kPa. These results show that the E of glomeruli is between 2 and 4 kPa. E of the GBM, 2.4 kPa, is consistent with this value, and is supported by the behavior of podocytes and mesangial cells grown on variable stiffness matrices. The podocyte cytoskeleton contributes the major component to the overall E of glomeruli, and a normal E requires ATP synthesis. The reduction in glomerular E following ischemia and in other diseases indicates that reduced glomerular E is a common feature of many forms of glomerular injury and indicative of an abnormal podocyte cytoskeleton.
登录
查看更多内容
DOI：
10.1083/jcb.146.4.831
发表时间：
1999-08-23
期刊：
The Journal of cell biology
影响因子：
--
作者：
Correia I;Chu D;Chou YH;Goldman RD;Matsudaira P
通讯作者：
Matsudaira P
影响因子：
18.2
作者：
Greka A;Mundel P
通讯作者：
Mundel P
影响因子：
2.4
作者：
Gladilin, Evgeny;Gonzalez, Paula;Eils, Roland
通讯作者：
Eils, Roland
影响因子：
19.6
作者：
GRANTHAM, JJ;DONOSO, VS;GARDNER, KD
通讯作者：
GARDNER, KD
影响因子：
3.7
作者：
Grin B;Mahammad S;Wedig T;Cleland MM;Tsai L;Herrmann H;Goldman RD
通讯作者：
Goldman RD