![]() ![]() There is no evidence for the presence of t-tubules in TE671RD cells, structures which would naturally confound simple geometric estimation of cellular volume in native skeletal muscle fibres. TE671RD cells are potentially an ideal model for cell volume regulation experiments because whilst they derive from human skeletal muscle they readily round-up and facilitate volume measurement. Different skeletal muscle fibre types have been shown to have differing propensity to undergo apoptosis in response to TNFα, but apoptosis in response to hypertonic challenge has not previously been investigated. ![]() It has therefore been hypothesised that apoptosis may contribute to sarcopenia in older people, potentially resulting from mitochondrial dysregulation. ![]() It has been argued that apoptosis is not necessarily pathological and is important for the process of remodelling, but it is increased subtly during ageing. The importance of apoptosis to ageing skeletal muscle physiology is controversial. Indeed, a number of genes critical to both cell volume control and apoptosis, including the AQP2 and AQP3 aquaporin channels, are differentially expressed in ageing skeletal muscle. Such chronic change in plasma osmotic potential of older people could therefore have a negative impact on skeletal muscle physiology, affecting such parameters as cellular volume. Cells are generally able to withstand small (2–3%) changes in tissue osmolality, but beyond this the activation of volume defence mechanisms becomes necessary. However, a loss in osmotic response is also observed in the elderly, suggesting that an issue with osmotic control could result in increased plasma osmolality. This could be due to changes in kidney function, as a result of hypertension, or due to environmental factors such as diet. Older people have an approximately 3% (302.2 compared with 291.2 mOsm/Kg H 2O) increased plasma osmolality compared to healthy younger people. Overall control of systemic osmolality is affected by a number of periventricular osmosensing structures within the brain and involves osmotic response of individual neurones by mechanisms analogous to that of cell volume regulation itself. In this study we investigate whether hypertonic challenge induces cell death in a human derived skeletal muscle cell line TE671RD. Hypertonic challenge can lead to apoptosis in a number of cell types. Frequently after cells reach a certain critical threshold of shrinkage, cells then undergo RVI or AVD. The first of these, RVI, is frequently involved with adaptation to hypertonic media and cell survival, whilst in some cells, but not others AVD leads to cell death. Regulatory volume increase (RVI) and apoptotic volume decrease (AVD) are two opposing cellular volume-regulatory mechanisms. ![]()
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