Polymorphism of the osteopontin gene and clinical course of multiple sclerosis in the Polish population.

Osteopontin (OPN) is a key cytokine involved in T-cell activation in multiple sclerosis (MS). We investigated whether polymorphism of the osteopontin gene affects MS occurrence and clinical course in a Polish population. Disability in 100 MS patients was evaluated using the Expanded Disability Status Scale (EDSS).

Interleukin 17 receptor in multiple sclerosis patients treated with interferon β-1a.

Interleukin 17 (IL-17) and its receptor IL-17R1 produced by T-helper cells named Th17 are involved in the pathology of autoimmune diseases. In contrast to the at least partially explained role of IL-17 in pathology of multiple sclerosis, the significance of IL-17R in MS is unclear. Therefore we have studied the expression of IL-17R in the stable phase of multiple sclerosis treated by interferon β-1a.

Impact of methylprednisolone treatment on the expression of macrophage inflammatory protein 3alpha and B lymphocyte chemoattractant in serum of multiple sclerosis patients.

In order to extend our studies designed to elucidate the mechanism of action of intravenous methylprednisolone (ivMP) in symptomatic therapy of relapses in multiple sclerosis (MS) victims, we have evaluated the expression of chemokines: macrophage inflammatory protein 3alpha (MIP-3alpha) and B-lymphocyte chemoattractant (CXCL13) before and after treatment. The data from further exploration of the MP mechanism of action in MS relapses may be helpful in establishing the treatment design, that would be specific both for individuals, and for the disease phase. The mean levels of MIP-3alpha in sera of MS patients showed no statistically significant differences compared to control subjects.

Effect of methylprednisolone treatment on expression of sPECAM-1 and CXCL10 chemokine in serum of MS patients.

In order to elucidate the mechanism of intravenous methylprednisolone (IVMP) therapy of relapses in multiple sclerosis (MS) patients, we have undertaken a study on the expression of the chemokines: soluble platelet endothelial cell adhesion molecule (sPECAM-1) and interferon gamma-inducible protein (CXCL10), before and after treatment. As more becomes known about the mechanism of methylprednisolone (MP) action, it may be possible to find a more specific treatment as well for the individual patients as the phase of the disease. The mean level of sPECAM-1 in our material was almost identical in either the MS and control subjects.

Steroidogenic factor 1 gene transcription is inhibited by transforming growth factor beta.

The orphan nuclear receptor, steroidogenic factor 1 (SF-1), plays a major role in adrenal and gonadal development, as well as in sexual differentiation. It has been demonstrated that the expression of a number of genes regulated by SF-1 is inhibited by the transforming growth factor, (TGF-beta). To date, however, the influence of TGF-beta on the expression of SF-1 gene has not been reported.

Temporal pattern of the induction of SF-1 gene expression by the signal transduction pathway involving 3',5'-cyclic adenosine monophosphate.

The objective of our study was to investigate the effect of stimulation of the cAMP-dependent pathway on the expression of an orphan nuclear receptor, SF-1/Ad4BP in mouse adrenal tumour, Y-1 cells in culture. We evaluated the temporal pattern of the effects of corticotropin (ACTH) and the adenylyl cyclase activator forskolin on the level of SF-1 mRNA, and compared the time course of induction of SF-1 with that of CYP11A1. Forskolin, corticotropin and 8-Br-cAMP significantly elevated the level of the SF-1 transcript, after 1.

Inhibition of CYP17 expression by adrenal androgens and transforming growth factor beta in adrenocortical cells.

Cytochrome P450c17, encoded by the CYP17 gene, is a component of the 17alpha-hydroxylase/17,20-lyase enzyme complex essential for production of adrenal glucocorticoids and androgens as well as gonadal androgens. The expression of CYP17 in adrenocortical cells is stimulated by corticotropin (ACTH) via the signal transduction pathway involving cAMP and protein kinase A (PKA). Thus, in addition to glucocorticoids, ACTH stimulates formation of adrenal androgens, which are known to induce transforming growth factor beta (TGF-beta) secretion.