Abstract
The influence of agonist (dexamethasone) and antagonist (mifepristone) of glucocorticoïd receptor during controllable painless stress was evaluated on myosin heavy chains expression in three masticatory and two nape rat muscles: anterior digastric (AD), anterior temporalis (AT), masseter superficialis (MS), longissimus capitis (L) and rectus capitis dorsalis major (R). The relative amounts of myosin heavy chain (MHC) protein isoform contained were significantly affected in four muscles studied by dexamethasone and in three muscles studied under mifepristone, versus control during the stress procedure, after only 1 week of treatment. The control group AT muscles contained respectively 18.2% of MHC 2A, 34.5% of MHC 2X and 47.4% of MHC 2B. The effects of dexamethasone and mifepristone were opposite in this muscle: under dexamethasone, the relative proportions of the three isoforms were 14.2, 31.0 and 54.8%: consequently, MHC 2A and 2X decreased with the profit of 2B. Under mifepristone, the relative proportions were 21.1, 36.6 and 42.3% (MHC 2A and 2X increased to the detriment of 2B). The L muscle was not affected by the two treatments and MS muscle was only affected by dexamethasone. Dexamethasone increased MHC 2B to the detriment of MHC 2A in MS, AD and R. Mifepristone and dexamethasone induced the same changes in AD. The mifepristone treatment decreased the MHC 2X profile in R. Under dexamethasone, four muscles exhibited a significantly higher proportion of the more rapid isoforms than under mifepristone. A previous work showed that controllable stress induced a marked increase in the relative expression of MHC 2B in the same skeletal muscles (Martrette et al., 1998). Our results confirm then a significant participation of glucocorticoïd in MHC isoform expression during controllable stress.
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Martrette, J.M., Hartmann, N., Westphal, A. et al. Effect of glucocorticoïd receptor ligands on myosin heavy chains expression in rat skeletal muscles during controllable stress. J Muscle Res Cell Motil 25, 297–302 (2004). https://doi.org/10.1007/s10974-004-4065-x
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DOI: https://doi.org/10.1007/s10974-004-4065-x