Role of nesprin-1 in nuclear deformation in endothelial cells under static and uniaxial stretching conditions

Toshiro Anno, Naoya Sakamoto, Masaaki Sato

Research output: Contribution to journalArticlepeer-review

25 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)94-99
Number of pages6
JournalBiochemical and biophysical research communications
Volume424
Issue number1
DOIs
Publication statusPublished - 2012 Jul 20

Keywords

  • Endothelial cells
  • Force transmission
  • LINC complex
  • Nesprin-1
  • Nucleus

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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