Biological aging modulates cell migration via lamin A/C-dependent nuclear motion

Jung Won Park, Seong Beom Han, Jungwon Hah, Geonhui Lee, Jeong Ki Kim, Soo Hyun Kim, Dong Hwee Kim

Research output: Contribution to journalArticle

Abstract

Aging is a progressive functional decline in organs and tissues over time and typically represents the accumulation of psychological and social changes in a human being. Diverse diseases, such as cardiovascular, musculoskeletal, and neurodegenerative disorders, are now understood to be caused by aging. While biological assessment of aging mainly focuses on the gradual changes that occur either on the molecular scale, for example, alteration of gene expression and epigenetic modification, or on larger scales, for example, changes in muscle strength and cardiac function, the mechanics that regulates the behavior of individual cells and interactions between the internal elements of cells, are largely missing. In this study, we show that the dynamic features of migrating cells across different human ages could help to establish the underlying mechanism of biological age-dependent cellular functional decline. To determine the relationship between cellular dynamics and human age, we identify the characteristic relationship between cell migration and nuclear motion which is tightly regulated by nucleus-bound cytoskeletal organization. This analysis demonstrates that actomyosin contractility-dependent nuclear motion plays a key role in cell migration. We anticipate this study to provide noble biophysical insights on biological aging in order to precisely diagnose age-related chronic diseases.

Original languageEnglish
Article number801
JournalMicromachines
Volume11
Issue number9
DOIs
Publication statusPublished - 2020 Sep

Keywords

  • Aging
  • Cell motility
  • Lamin A/C
  • Nuclear dynamics

ASJC Scopus subject areas

  • Control and Systems Engineering
  • Mechanical Engineering
  • Electrical and Electronic Engineering

Fingerprint Dive into the research topics of 'Biological aging modulates cell migration via lamin A/C-dependent nuclear motion'. Together they form a unique fingerprint.

  • Cite this