• 제목/요약/키워드: 세포 군집 운동

검색결과 3건 처리시간 0.014초

세포군집의 확장에 관여하는 물리적 힘의 가시화 (Visualization of mechanical stresses in expanding cell cluster)

  • 조영빈;권보미;고웅현;신현정
    • 한국가시화정보학회지
    • /
    • 제13권1호
    • /
    • pp.43-48
    • /
    • 2015
  • Collective cell migration is a fundamental phenomenon observed in various biological processes such as development, wound healing, and cancer metastasis. During the collective migration, cells undergo changes in their phenotypes from those of stable to the migratory state via the process called epithelial-mesenchymal transition (EMT). Recent findings in biology and biochemistry have shown that EMT is closely related to the cancer invasion or metastasis, but not much of the correlations in kinematics and physical forces between the neighboring cells are known yet. In this study, we aim to understand the cell migration and stress distribution within the expanding cell cluster. We constructed the in vitro cell cluster on the hydrogel, employed traction force microscopy (TFM) and monolayer stress microscopy (MSM) to visualize the physical forces within the expanding cell monolayer. During the expansion, cells at the cluster edge exhibited enhanced motility and developed focal adhesions that are the essential features of EMT while cells at the core of the cluster maintained the epithelial characteristics. In the aspect of mechanical stress, the cluster edge had the highest traction force of ~90 Pa directed toward the cluster core, which means that cells at the edge actively pull the substrate to make the cluster expansion. The cluster core of the tightly confined cells by neighboring cells had a lower traction force value (~60 Pa) but the highest intercellular normal stress of ~800 Pa because of the accumulation of traction from the edge of the monolayer.

세포 재밍 과정의 역학적 상관 관계 가시화 (Visualization of Dynamic Correlations during Cellular Jamming)

  • 정현태;조영빈;신현정
    • 한국가시화정보학회지
    • /
    • 제16권2호
    • /
    • pp.38-44
    • /
    • 2018
  • Cellular jamming phenomenon, defined as a kinetic arrest, is a commonly observed event in dense cell aggregates in epithelial tissues. Cells lose their motility when the density of the cell population becomes too high. Yet, not much is known about how the jamming occurs and how it influences individual cells in the population. In this study, we investigated the mechanisms during the formation of the jammed state by visualizing various dynamic components such as velocity, traction, and intercellular stress. The visualized properties exhibited interrelated features in similar time domains that can be categorized into specific stages, namely migrating, transitional and steady state. During the migrating stage, cells generated spatially correlated tractions and migrations at the collective migration step and lost these properties becoming a transitional stage. These stepwise analyses presented correlative components which are expected to adjust for explaining the detailed mechanisms of cellular jamming.

세포 운동 가시화를 통한 상처 치유 과정 내 경계 이동의 규명 (Identification of boundary migration during the wound healing through the visualization of cell migrations)

  • 정현태;이재성;신현정
    • 한국가시화정보학회지
    • /
    • 제18권2호
    • /
    • pp.10-17
    • /
    • 2020
  • The curvature of wound boundaries has been identified as a key modulator that determines a type of force responsible for cell migration. While several studies report how certain curvatures of the boundary correlate with the rate at which the wound closes, it remains unclear how these curvatures are spatiotemporally formed to regulate the healing process. We investigated the dynamic changes in the boundary curvatures by visualizing cell migration patterns. Locally, cells at the convex boundary continuously move forward with transmitting kinetic responses behind to the cells away from the boundary, and cells at the concave boundary exhibit dramatic contracting motion, like a purse-string, when they accumulate enough negative curvatures to gain the thrust toward the void. Globally, the dynamics of boundary geometries are controlled by the diffusive flow of cells driven by the density gradient between the wound area and the cell layer.