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

Authors
Kim, Tae-JinJoo, ChirlminSeong, JihyeVafabakhsh, RezaBotvinick, Elliot L.Berns, Michael W.Palmer, Amy E.Wang, NingHa, TaekjipJakobsson, EricSun, JieWang, Yingxiao
Issue Date
2015-02-10
Publisher
ELIFE SCIENCES PUBLICATIONS LTD
Citation
ELIFE, v.4
Abstract
It is unclear that how subcellular organelles respond to external mechanical stimuli. Here, we investigated the molecular mechanisms by which mechanical force regulates Ca2+ signaling at endoplasmic reticulum (ER) in human mesenchymal stem cells. Without extracellular Ca2+, ER Ca2+ release is the source of intracellular Ca2+ 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 ER Ca2+ 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 mechanosensitive Ca2+ 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.
Keywords
INTRACELLULAR CALCIUM-RELEASE; MECHANOSENSITIVE ION CHANNELS; MESENCHYMAL STEM-CELLS; SMOOTH-MUSCLE-CELLS; LIGHT-CHAIN KINASE; T-LYMPHOMA CELLS; NITRIC-OXIDE; MOLECULAR-BASIS; IP3 RECEPTORS; LIVING CELLS; INTRACELLULAR CALCIUM-RELEASE; MECHANOSENSITIVE ION CHANNELS; MESENCHYMAL STEM-CELLS; SMOOTH-MUSCLE-CELLS; LIGHT-CHAIN KINASE; T-LYMPHOMA CELLS; NITRIC-OXIDE; MOLECULAR-BASIS; IP3 RECEPTORS; LIVING CELLS
ISSN
2050-084X
URI
https://pubs.kist.re.kr/handle/201004/125769
DOI
10.7554/eLife.04876
Appears in Collections:
KIST Article > 2015
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