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Thread: Estrada, et al. (2003). Testosterone stimulates intracellular calcium release and mitogen-activated protein kinases via a g protein-coupled receptor in skeletal muscle cells.

  1. #1

    Estrada, et al. (2003). Testosterone stimulates intracellular calcium release and mitogen-activated protein kinases via a g protein-coupled receptor in skeletal muscle cells.

    • Estrada M, Espinosa A, Muller M and Jaimovich E (2003). Testosterone stimulates intracellular calcium release and mitogen-activated protein kinases via a g protein-coupled receptor in skeletal muscle cells. Endocrinology 144:3586-97. Summary: Involvement of intracellular Ca(2+) and ERK1/2 phosphorylation in the fast nongenomic effects of androgens in myotubes was investigated. Testosterone or nandrolone produced fast (<1 min) and transient increases in intracellular Ca[2+) with an oscillatory pattern. Calcium signals were slightly reduced in Ca[2+)-free medium, but lack of oscillations was evident. Signals were blocked by U-73122 and xestospongin B, inhibitors of inositol 1,4,5-trisphosphate [IP[3)) pathway. Furthermore, IP[3) increased transiently 2- to 3-fold 45 sec after hormone addition. Cyproterone neither affected the fast Ca[2+) signal nor the increase in IP[3). Calcium increases could also be induced by the impermeant testosterone conjugated to BSA, and the effect of testosterone was abolished in cells incubated with guanosine 5'-O-[2-thiodiphosphate) or pertussis toxin. Stimulation of myotubes with testosterone, nandrolone, or testosterone conjugated to BSA increased immunodetectable phosphorylation of ERK1/2 within 5 min, and this effect was not inhibited by cyproterone. Phosphorylation was blocked by the use of 1,2-bis[2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethylester, U-73122, and xestospongin B as well as by dominant negative Ras, MAPK kinase [MEK), or the MEK inhibitor PD-98059. In addition, guanosine 5'-O-[2-thiodiphosphate) or pertussis toxin blocked ERK1/2 phosphorylation. These results are consistent with a fast effect of testosterone, involving a G protein-linked receptor at the plasma membrane, IP[3)-mediated Ca[2+) signal, and the Ras/MEK/ERK pathway in muscle cells. Centro de Estudios Moleculares de la Celula and Instituto de Ciencias Biomedicas, Facultad de Medicina, Universidad de Chile, Casilla 70005, Santiago 6530499, Chile.

  2. #2
    • Bouhlel A, Joumaa WH and Leoty C (2003). Nandrolone decanoate treatment affects sarcoplasmic reticulum Ca(2+) ATPase function in skinned rat slow- and fast-twitch fibres. Pflugers Arch Summary: The effects of anabolic-androgenic steroid administration on the function of the sarcoplasmic reticulum (SR) pump were investigated in chemically skinned fibres from the extensor digitorum longus (EDL) and soleus muscles of sedentary rats. Twenty male rats were divided into two groups, one group received an intramuscular injection of nandrolone decanoate (15 mg kg(-1)) weekly for 8 weeks, the second received similar weekly doses of vehicle (sterile peanut oil). Compared with control muscles, nandrolone decanoate treatment reduced SR Ca(2+) loading in EDL and soleus fibres by 49% and 29%, respectively. In control and treated muscles, the rate of Ca(2+) leakage depended on the quantity of Ca(2+) loaded. Furthermore, for similar SR Ca(2+) contents, the Ca(2+) leakage rate was not significantly modified by nandrolone decanoate treatment. Nandrolone decanoate treatment thus affects Ca (2+) uptake by the SR in a fibre-type dependent manner. Laboratoire de Physiologie Generale, UMR CNRS 6018, Faculte des Sciences et des Techniques, Universite de Nantes, 2 rue de la Houssiniere, B.P. 92208, 44322, Nantes Cedex 3, France.

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