کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1929373 | 1050453 | 2012 | 6 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Role of nesprin-1 in nuclear deformation in endothelial cells under static and uniaxial stretching conditions Role of nesprin-1 in nuclear deformation in endothelial cells under static and uniaxial stretching conditions](/preview/png/1929373.png)
The linker of nucleus and cytoskeleton (LINC) complex, including nesprin-1, has been suggested to be crucial for many biological processes. Previous studies have shown that mutations in nesprin-1 cause abnormal cellular functions and diseases, possibly because of insufficient force transmission to the nucleus through actin filaments (F-actin) bound to nesprin-1. However, little is known regarding the mechanical interaction between the nucleus and F-actin through nesprin-1. In this study, we examined nuclear deformation behavior in nesprin-1 knocked-down endothelial cells (ECs) subjected to uniaxial stretching by evaluating nuclear strain from lateral cross-sectional images. The widths of nuclei in nesprin-1 knocked-down ECs were smaller than those in wild-type cells. In addition, nuclear strain in nesprin-1 knocked-down cells, which is considered to be compressed by the actin cortical layer, increased compared with that in wild-type cells under stretching condition. These results indicate that nesprin-1 knockdown releases the nucleus from the tension of F-actin bound to the nucleus, thereby increasing allowance for deformation before stretching, and that F-actin bound to the nucleus through nesprin-1 causes sustainable force transmission to the nucleus.
► Nesprin-1 knockdown decreases widths of nuclei in ECs under static condition.
► Nuclear strain caused by stretching is increased by nesprin-1 knockdown in ECs.
► We model mechanical interactions of F-actin with the nucleus in stretched cells.
► F-actin bound to nesprin-1 may cause sustainable force transmission to the nucleus.
Journal: Biochemical and Biophysical Research Communications - Volume 424, Issue 1, 20 July 2012, Pages 94–99