Intracellular Ca²⁺ signaling is a key regulator of proliferation, cell cycle progression and apoptosis. The plasma membrane Ca²⁺-ATPase (PMCA), encoded by four separate genes, is a crucial controller of intracellular calcium signaling. Steroid hormones belong to physiologically important direct or indirect regulators of calcium pump activity. Steroids produced in the CNS (neurosteroids) in most cases are neuroactive and play an important role in many brain functions through genomic and non-genomic action. While action of steroids at the genome requires a time period from minutes to hours limited by the rate of protein biosynthesis, the modulatory effects of neuroactive steroids are faster occurring events within milliseconds to seconds. Thus, the genomic and nongenomic effects of steroids within the central nervous system provide the molecular basis for a broad spectrum of steroid action on neuronal function and plasticity. Neurosteroids appears to participate in the membrane enzymes activity regulation, playing crucial role in maintenance of neuronal calcium homeostasis. PC12 cell line is a suitable and frequently used model for the study on neurotransmission, including Ca²⁺ signaling. To evaluate the potential role of neuron-specific PMCA isoforms in maintaince of calcium homeostasis, we have constructed the stably transfected PC12 cell lines, with suppressed expression of PMCA 2 and PMCA3. The aim of presented study was to elucidate the influence of selected steroid hormones on PMCA transport activity in control and transfected PC12 cell lines. Analysis of short term action of 17-α-estradiol and 17-β-estradiol at physiological and pharmacological concentrations showed that transport of calcium ions is modulated in non genomic manner on plasma membrane level, and this effect appeared to be dependent on PMCAs composition.

Supported by the grants No: PBZ-MIN-012/P04/2004 and 2/P05A/03529 from the Ministry of Education and Science, and 503-6086-2 from the Medical University of Lodz.

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