Department of Biomedical Engineering, Washington University, St. Louis, Missouri, USA.
Biophys J. 2010 Apr 21;98(8):1685-93. doi: 10.1016/j.bpj.2009.12.4324.
Von Willebrand factor (VWF) is a multimeric plasma glycoprotein involved in both hemostasis and thrombosis. VWF conformational changes, especially unfolding of the A2 domain, may be required for efficient enzymatic cleavage in vivo. It has been shown that a single A2 domain unfolds at most probable unfolding forces of 7-14 pN at force loading rates of 0.35-350 pN/s and A2 unfolding facilitates A2 cleavage in vitro. However, it remains unknown how much force is required to unfold the A2 domain in the context of a VWF multimer where A2 may be stabilized by other domains like A1 and A3. With the optical trap, we stretched VWF multimers and a poly-protein (A1A2A3)3 that contains three repeats of the triplet A1A2A3 domains at constant speeds of 2000 nm/s and 400 nm/s, respectively, which yielded corresponding average force loading rates of 90 and 22 pN/s. We found that VWF multimers became stiffer when they were stretched and extended by force. After force increased to a certain level, sudden extensional jumps that signify domain unfolding were often observed. Histograms of the unfolding force and the unfolded contour length showed two or three peaks that were integral multiples of approximately 21 pN and approximately 63 nm, respectively. Stretching of (A1A2A3)3 yielded comparable distributions of unfolding force and unfolded contour length, showing that unfolding of the A2 domain accounts for the behavior of VWF multimers under tension. These results show that the A2 domain can be indeed unfolded in the presence of A1, A3, and other domains. Compared with the value in the literature, the larger most probable unfolding force measured in this study suggests that the A2 domain is mechanically stabilized by A1 or A3 although variations in experimental setups and conditions may complicate this interpretation.
血管性血友病因子(VWF)是一种参与止血和血栓形成的多聚体血浆糖蛋白。VWF 构象变化,特别是 A2 结构域的展开,可能是体内酶切的有效条件。研究表明,在 0.35-350 pN/s 的力加载速率下,A2 结构域最多只能展开 7-14 pN 的最可能展开力,并且 A2 结构域的展开有利于体外 A2 结构域的切割。然而,在 VWF 多聚体的情况下,A2 结构域需要展开多少力仍然未知,在 VWF 多聚体中,A2 结构域可能被其他结构域(如 A1 和 A3)稳定。在光学阱中,我们以 2000nm/s 和 400nm/s 的恒定速度分别拉伸 VWF 多聚体和包含三个 A1A2A3 结构域重复的三聚体(A1A2A3)3,这分别产生相应的平均力加载速率为 90 和 22 pN/s。我们发现,当 VWF 多聚体受到力的拉伸和延伸时,它们会变得更硬。当力增加到一定水平时,通常会观察到突然的伸展跳跃,这表明结构域的展开。展开力和展开轮廓长度的直方图显示出两个或三个峰,分别是大约 21 pN 和大约 63nm 的整数倍。(A1A2A3)3 的拉伸产生了类似的展开力和展开轮廓长度分布,表明 A2 结构域的展开解释了 VWF 多聚体在张力下的行为。这些结果表明,在 A1、A3 和其他结构域的存在下,A2 结构域确实可以展开。与文献中的值相比,本研究中测量的较大的最可能展开力表明,尽管实验设置和条件的变化可能使这种解释复杂化,但 A2 结构域在机械上受到 A1 或 A3 的稳定。