Key result
Transforming growth factor beta-1 inhibited isoproterenol-induced intracellular calcium elevation and decreased beta-adrenergic receptor number by approximately 53% in cultured rat cardiac fibroblasts.
Why the study?
Does transforming growth factor beta-1 modulate intracellular calcium and beta-adrenergic signal transduction in cardiac fibroblasts?
Does transforming growth factor beta-1 modulate intracellular calcium and beta-adrenergic signal transduction in cardiac fibroblasts?
TGF-beta-1 modulates beta-adrenergic signal transduction and intracellular calcium concentration by downregulating the number of beta-adrenergic receptors in cardiac fibroblasts, suggesting a potential cardioprotective mechanism against calcium overload.
TGF-β1 may modulate fibroblast calcium handling; leaves open any role in human cardiac remodeling or therapy.
We attempted to determine the effects of transforming growth factor beta-1 on intracellular Ca2+ concentration changes in the presence of isoproterenol in cardiac fibroblasts. Transforming growth factor beta-1 inhibited the increase of intracellular Ca2+ concentration in the presence of isoproterenol in fibroblasts. It also inhibited the production of cyclic-AMP in fibroblasts in the presence of isoproterenol. Islet-activating protein did not block these reactions of transforming growth factor beta-1. Forskolin did not affect the intracellular calcium concentration change resulting from treatment with transforming growth factor beta-1. Binding of [3H]CGP-12177 was decreased to 47% of control preincubated for 24 hours with transforming growth factor beta-1 in fibroblasts. Scatchard plots suggested a decrease in beta-adrenergic receptor number without specific change in receptor affinity. These results suggested that transforming growth factor beta-1 modulates the signal transduction through beta-adrenergic receptor and intracellular Ca2+ concentration by regulating the number of receptors in fibroblasts.
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Iizuka et al. (1995) studied None (healthy Wistar rat cardiac fibroblasts). Transforming growth factor beta-1 vs. Control (no TGF-beta-1) was evaluated on Intracellular calcium concentration change and beta-adrenergic receptor number (p=<0.001). Transforming growth factor beta-1 inhibited isoproterenol-induced intracellular calcium elevation and decreased beta-adrenergic receptor number by approximately 53% in cultured rat cardiac fibroblasts.
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