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Molecular basis of mechanisms of steroid resistance in children with nephrotic syndrome

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Świerczewska M., Ostalska-Nowicka D., Kempisty B., Nowicki M., Zabel M.

2013

vol. 60

issue 3

339-344

Steroid therapy, due to a wide range of anti-inflammatory properties of steroids, is a basic field of treatment in many human diseases including the nephrotic syndrome in children. However, not all patients respond positively to therapy which divides them into steroid sensitive (SS) and steroid resistance (SR) individuals. Many potential factors associated with steroid resistance have been identified so far. It seems that genetic factors associated with glucocorticoid receptor α (GRα), the structure of heterocomplex of GR as well as glycoprotein P or cytochrome P450 may play a role in the induction of glucocorticoid resistance. Here we described several of the molecular mechanisms, which can regulate glucocorticoid sensitivity and resistance. Moreover, we presented genetic defects, which can lead to various effects of treatment and, in a longer perspective, enable clinicians to individualize therapies.

Identification and tissue distribution of a novel rat glucocorticoid receptor splice variant

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Ju H., Wang X., Liu Z., Liu P., Zhao Y., Xiong R., Zhou Y., Chen X.

Glucocorticoid receptor (GR) is a steroid hormone receptor that has been shown to play important roles in diverse cellular and physiological processes. More and more evidence has revealed that the effects of glucocorticoids are mediated by the glucocorticoid receptor through genomic or nongenomic mechanisms. A growing number of glucocorticoid receptor splice variants have been identified in human tissues, but few are known in rat tissues. In this work, a novel rGR cDNA, called rGRβ, was cloned from Sprague Dawlay (SD) rat liver. Sequence analysis revealed that the rGRβ mRNA was 39 base pairs (bp) shorter than the rGR mRNA reported earlier. The deleted segment is located in exon 1 and encodes 13 repeated glutamine residues. Both the rGR and rGRβ mRNAs were quantitated by Northern blot hybridization using non-homologous glucocorticoid cDNA probes. Results showed that the rGR and rGRβ mRNAs were most abundant in the lung, the least abundant in the heart, and there were more rGR and rGRβ mRNAs in the kidney than in the liver. The identification of rGRβ may contribute to the understanding of the genomic or nongenomic effects of glucocorticoids.

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2 Acta Biochimica Polonica

1 2013

1 2009

1 Chen X.

1 Ju H.

1 Kempisty B.

1 Liu P.

1 Liu Z.

1 Nowicki M.

1 Ostalska-Nowicka D.

1 Wang X.

1 Xiong R.

1 Zabel M.

1 Zhao Y.

1 Zhou Y.

1 Świerczewska M.

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Molecular basis of mechanisms of steroid resistance in children with nephrotic syndrome

Identification and tissue distribution of a novel rat glucocorticoid receptor splice variant