ECM stiffness regulates calcium influx into mitochondria via tubulin and VDAC1 activity

Calcium ions (Ca 2+ ) play pivotal roles in regulating numerous cellular functions, including metabolism and growth, in normal and cancerous cells. Consequently, Ca 2+ signaling is a vital determinant of cell fate and influences both cell survival and death. These intracellular signals are susceptib...

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Published in:Animal cells and systems 2024, 28(1), , pp.417-427
Main Authors: Kim, Minji, Han, Kiseok, Choi, Gyuho, Ahn, Sanghyun, Suh, Jung-Soo, Kim, Tae-Jin
Format: Article
Language:English
Subjects:
Biosensors
Calcium
Calcium (extracellular)
Calcium (intracellular)
Calcium (mitochondrial)
Calcium (reticular)
Calcium channels (voltage-gated)
Calcium homeostasis
Calcium imaging
Calcium influx
Calcium ions
Calcium metabolism
Calcium signalling
Cell death
Cell fate
Cell survival
ECM stiffness
Endoplasmic reticulum
Extracellular matrix
Genetic code
Homeostasis
Intracellular
Intracellular signalling
Ion channels
live cell imaging
Mechanical properties
Mitochondria
Regulatory mechanisms (biology)
Stiffness
Tubulin
VDAC1
생물학
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container_issue 1
container_start_page 417
container_title Animal cells and systems
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creator Kim, Minji
Han, Kiseok
Choi, Gyuho
Ahn, Sanghyun
Suh, Jung-Soo
Kim, Tae-Jin
description Calcium ions (Ca 2+ ) play pivotal roles in regulating numerous cellular functions, including metabolism and growth, in normal and cancerous cells. Consequently, Ca 2+ signaling is a vital determinant of cell fate and influences both cell survival and death. These intracellular signals are susceptible to modulation by various factors, including changes in the extracellular environment, which leads to mechanical alterations. However, the effect of extracellular matrix (ECM) stiffness variations on intracellular Ca 2+ signaling remains underexplored. In this study, we aimed to elucidate the mechanisms of Ca 2+ regulation through the mitochondria, which are crucial to Ca 2+ homeostasis. We investigated how Ca 2+ regulatory mechanisms adapt to different levels of ECM stiffness by simultaneously imaging the mitochondria and endoplasmic reticulum (ER) in live cells using genetically encoded biosensors. Our findings revealed that the uptake of mitochondrial Ca 2+ through Voltage-Dependent Anion Channel 1 (VDAC1), facilitated by intracellular tubulin, is influenced by ECM stiffness. Unraveling these Ca 2+ regulatory mechanisms under various conditions offers a novel perspective for advancing biomedical studies involving Ca 2+ signaling.
doi_str_mv 10.1080/19768354.2024.2393811
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subjects Biosensors
Calcium
Calcium (extracellular)
Calcium (intracellular)
Calcium (mitochondrial)
Calcium (reticular)
Calcium channels (voltage-gated)
Calcium homeostasis
Calcium imaging
Calcium influx
Calcium ions
Calcium metabolism
Calcium signalling
Cell death
Cell fate
Cell survival
ECM stiffness
Endoplasmic reticulum
Extracellular matrix
Genetic code
Homeostasis
Intracellular
Intracellular signalling
Ion channels
live cell imaging
Mechanical properties
Mitochondria
Regulatory mechanisms (biology)
Stiffness
Tubulin
VDAC1
생물학
title ECM stiffness regulates calcium influx into mitochondria via tubulin and VDAC1 activity
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