Distinct mechanisms regulating mechanical force-induced Ca²⁺ signals at the plasma membrane and the ER in human MSCs
Autor: | Kim, Tae-Jin, Joo, Chirlmin, Seong, Jihye, Vafabakhsh, Reza, Botvinick, Elliot L, Berns, Michael W, Palmer, Amy E, Wang, Ning, Ha, Taekjip, Jakobsson, Eric, Sun, Jie, Wang, Yingxiao |
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Rok vydání: | 2015 |
Předmět: |
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1.1 Normal biological development and functioning Intracellular Space Bioengineering Biosensing Techniques Endoplasmic Reticulum Transfection Stress FRET biosensor developmental biology Underpinning research stem cells biophysics optical laser tweezers Fluorescence Resonance Energy Transfer Animals Humans structural biology Calcium Signaling mechanical stimulation Cytoskeleton mesenchymal stem cells calcium signals Mesenchymal Stromal Cells Cell Membrane Actomyosin Mechanical molecular imaging Cattle Calcium Generic health relevance Biochemistry and Cell Biology |
Zdroj: | eLife, vol 4, iss 4 |
Popis: | It is unclear that how subcellular organelles respond to external mechanical stimuli. Here, we investigated the molecular mechanisms by which mechanical force regulates Ca(2+) signaling at endoplasmic reticulum (ER) in human mesenchymal stem cells. Without extracellular Ca(2+), ER Ca(2+) release is the source of intracellular Ca(2+) 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 Ca(2+) release upon mechanical stimulation is mediated not only by the mechanical support of cytoskeleton and actomyosin contractility, but also by mechanosensitive Ca(2+) permeable channels on the plasma membrane, specifically TRPM7. However, Ca(2+) influx at the plasma membrane via mechanosensitive Ca(2+) 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. |
Databáze: | OpenAIRE |
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