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.
Highlights
Aging is a complex and multifaceted time-dependent biological process associated with the decline of cellular functions, onset of diverse diseases, and incremental risk of death [1]
The distance of retraction of the actin stress fiber was 1.7-times larger in young Human dermal fibroblast (HDF) (5.44 μm) than in old HDF (3.17 μm) after 15 s of laser ablation (Figure 4G), i.e., actin cytoskeleton retraction was faster in young HDFs. These results indicate that cytoskeletal tension in young HDFs is higher than in old HDFs, and actomyosin contractility becomes weaker as the expression of lamin A/C diminishes with the aging process
These studies demonstrate that cell and nuclear dimensions that are tightly connected to modification of cell motility are altered in a highly predictive manner as biological aging progresses
Summary
Aging is a complex and multifaceted time-dependent biological process associated with the decline of cellular functions, onset of diverse diseases, and incremental risk of death [1]. Accumulation of organ-specific aging processes causes progression of cardiovascular, musculoskeletal, and neurodegenerative disorders, as well as, various chronic diseases, such as diabetes, hypertension, and Alzheimer’s disease [2]. Previous studies involving aging have mainly focused on phenotypic alterations at the organ and tissue level or dysfunction of multicellular organs, for example, reduction of mechanical strength, barrier function, and energy production in aged skin [4], and a dramatic decline of cardiovascular function in aged heart [5]. The mechanism of how biological aging determines the dynamic motion of individual cells that play a critical role in organ-specific functionality is not yet clearly identified
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