Osmotic pressure modulates single cell cycle dynamics inducing reversible growth arrest and reactivation of human metastatic cells

Publikation: Beitrag in FachzeitschriftForschungsartikelBeigetragenBegutachtung

Beitragende

  • Hubert M. Taïeb - , Max Planck Institute of Colloids and Interfaces (Autor:in)
  • Daniela S. Garske - , Max Planck Institute of Colloids and Interfaces (Autor:in)
  • Jörg Contzen - , Charité – Universitätsmedizin Berlin, Helmholtz-Zentrum Hereon (Autor:in)
  • Manfred Gossen - , Helmholtz-Zentrum Hereon, Charité – Universitätsmedizin Berlin (Autor:in)
  • Luca Bertinetti - , Max Planck Institute of Colloids and Interfaces (Autor:in)
  • Tom Robinson - , Max Planck Institute of Colloids and Interfaces (Autor:in)
  • Amaia Cipitria - , Max Planck Institute of Colloids and Interfaces (Autor:in)

Abstract

Biophysical cues such as osmotic pressure modulate proliferation and growth arrest of bacteria, yeast cells and seeds. In tissues, osmotic regulation takes place through blood and lymphatic capillaries and, at a single cell level, water and osmoregulation play a critical role. However, the effect of osmotic pressure on single cell cycle dynamics remains poorly understood. Here, we investigate the effect of osmotic pressure on single cell cycle dynamics, nuclear growth, proliferation, migration and protein expression, by quantitative time-lapse imaging of single cells genetically modified with fluorescent ubiquitination-based cell cycle indicator 2 (FUCCI2). Single cell data reveals that under hyperosmotic stress, distinct cell subpopulations emerge with impaired nuclear growth, delayed or growth arrested cell cycle and reduced migration. This state is reversible for mild hyperosmotic stress, where cells return to regular cell cycle dynamics, proliferation and migration. Thus, osmotic pressure can modulate the reversible growth arrest and reactivation of human metastatic cells.

Details

OriginalspracheEnglisch
Aufsatznummer13455
FachzeitschriftScientific reports
Jahrgang11
Ausgabenummer1
PublikationsstatusVeröffentlicht - Dez. 2021
Peer-Review-StatusJa
Extern publiziertJa

Externe IDs

PubMed 34188099
ORCID /0000-0002-4666-9610/work/142238928

Schlagworte

ASJC Scopus Sachgebiete