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Changes in intracellular calcium during compression of C2C12 myotubes

Changes in intracellular calcium during compression of C2C12 myotubes
Changes in intracellular calcium during compression of C2C12 myotubes
In recent years, damage directly due to tissue deformation has gained interest in deep pressure ulcer aetiology research. It has been shown that deformation causes muscle cell damage, though the pathway is unclear. Mechanically induced skeletal muscle damage has often been associated with an increased intracellular Ca2+ concentration, e.g. in eccentric exercise (Allen et al., J Physiol 567(3):723–735, 2005). Therefore, the hypothesis was that compression leads to membrane disruptions, causing an increased Ca2+-influx, eventually leading to Ca2+ overload and cell death. Monolayers of differentiated C2C12 myocytes, stained with a calcium-sensitive probe (fluo-4), were individually subjected to compression while monitoring the fluo-4 intensity. Approximately 50% of the cells exhibited brief calcium transients in response to compression, while the rest did not react. However, all cells demonstrated a prolonged Ca2+ up-regulation upon necrosis, which induced similar up-regulations in some of the surrounding cells. Population heterogeneity is a possible explanation for the observed differences in response, and it might also become important in tissue damage development. It did not become clear however whether Ca2+-influxes were the initiators of damage
pressure ulcers, aetiology, deformation, injury, skeletal muscle
1741-2765
25-33
Ceelen, K.K.
3e9d84ab-1fa2-4b31-9883-c9076b001d68
Oomens, C.W.J.
a8310c52-8ab4-4652-b2d6-82269a3c7438
Stekelenburg, A.
81bba22a-0eb4-48fa-9504-2faa5c174366
Bader, D.L.
9884d4f6-2607-4d48-bf0c-62bdcc0d1dbf
Baaijens, F.P.T.
5d9e63e2-7d7b-4f64-b942-29121121dce0
Ceelen, K.K.
3e9d84ab-1fa2-4b31-9883-c9076b001d68
Oomens, C.W.J.
a8310c52-8ab4-4652-b2d6-82269a3c7438
Stekelenburg, A.
81bba22a-0eb4-48fa-9504-2faa5c174366
Bader, D.L.
9884d4f6-2607-4d48-bf0c-62bdcc0d1dbf
Baaijens, F.P.T.
5d9e63e2-7d7b-4f64-b942-29121121dce0

Ceelen, K.K., Oomens, C.W.J., Stekelenburg, A., Bader, D.L. and Baaijens, F.P.T. (2009) Changes in intracellular calcium during compression of C2C12 myotubes. Experimental Mechanics, 49 (1), 25-33. (doi:10.1007/s11340-007-9093-1).

Record type: Article

Abstract

In recent years, damage directly due to tissue deformation has gained interest in deep pressure ulcer aetiology research. It has been shown that deformation causes muscle cell damage, though the pathway is unclear. Mechanically induced skeletal muscle damage has often been associated with an increased intracellular Ca2+ concentration, e.g. in eccentric exercise (Allen et al., J Physiol 567(3):723–735, 2005). Therefore, the hypothesis was that compression leads to membrane disruptions, causing an increased Ca2+-influx, eventually leading to Ca2+ overload and cell death. Monolayers of differentiated C2C12 myocytes, stained with a calcium-sensitive probe (fluo-4), were individually subjected to compression while monitoring the fluo-4 intensity. Approximately 50% of the cells exhibited brief calcium transients in response to compression, while the rest did not react. However, all cells demonstrated a prolonged Ca2+ up-regulation upon necrosis, which induced similar up-regulations in some of the surrounding cells. Population heterogeneity is a possible explanation for the observed differences in response, and it might also become important in tissue damage development. It did not become clear however whether Ca2+-influxes were the initiators of damage

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Published date: February 2009
Keywords: pressure ulcers, aetiology, deformation, injury, skeletal muscle

Identifiers

Local EPrints ID: 189283
URI: http://eprints.soton.ac.uk/id/eprint/189283
ISSN: 1741-2765
PURE UUID: 62c2e212-f2c9-4548-af25-c968268c4cf3
ORCID for D.L. Bader: ORCID iD orcid.org/0000-0002-1208-3507

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Date deposited: 02 Jun 2011 10:20
Last modified: 14 Mar 2024 03:35

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Contributors

Author: K.K. Ceelen
Author: C.W.J. Oomens
Author: A. Stekelenburg
Author: D.L. Bader ORCID iD
Author: F.P.T. Baaijens

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