Distinct mechanisms regulating mechanical force-induced Ca2+ signals at the plasma membrane and the ER in human MSCs

Tae Jin Kim, Chirlmin Joo, Jihye Seong, Reza Vafabakhsh, Elliot L. Botvinick, Michael W. Berns, Amy E. Palmer, Ning Wang, Taekjip Ha, Eric Jakobsson, Jie Sun, Yingxiao Wang

Research output: Contribution to journalArticlepeer-review


It is unclear that how subcellular organelles respond to external mechanical stimuli. Here, we investigated the molecular mechanisms by which mechanical force regulatesCa2+ signaling at endoplasmic reticulum (ER) in human mesenchymal stem cells. Without extracellularCa2+, ERCa2+ release is the source of intracellularCa2+ oscillations induced by laser-tweezer-traction at the plasma membrane, providing a model to study how mechanical stimuli can be transmitted deep inside the cell body. This ERCa2+ release upon mechanical stimulation is mediated not only by the mechanical support of cytoskeleton and actomyosin contractility, but also by mechanosensitive Ca2+ permeable channels on the plasma membrane, specifically TRPM7. However,Ca2+ influx at the plasma membrane via mechanosensitiveCa2+ permeable channels is only mediated by the passive cytoskeletal structure but not active actomyosin contractility. Thus, active actomyosin contractility is essential for the response of ER to the external mechanical stimuli, distinct from the mechanical regulation at the plasma membrane.

Original languageEnglish (US)
Article numbere04876
Issue number4
StatePublished - Feb 10 2015

ASJC Scopus subject areas

  • Neuroscience(all)
  • Immunology and Microbiology(all)
  • Biochemistry, Genetics and Molecular Biology(all)


Dive into the research topics of 'Distinct mechanisms regulating mechanical force-induced Ca<sup>2+</sup> signals at the plasma membrane and the ER in human MSCs'. Together they form a unique fingerprint.

Cite this