| First Author | Dawson PA | Year | 2008 |
| Journal | J Steroid Biochem Mol Biol | Volume | 112 |
| Issue | 1-3 | Pages | 55-62 |
| PubMed ID | 18790054 | Mgi Jnum | J:142521 |
| Mgi Id | MGI:3821655 | Doi | 10.1016/j.jsbmb.2008.08.003 |
| Citation | Dawson PA, et al. (2008) Kidney transcriptome reveals altered steroid homeostasis in NaS1 sulfate transporter null mice. J Steroid Biochem Mol Biol 112(1-3):55-62 |
| abstractText | Sulfate is essential for human growth and development, and circulating sulfate levels are maintained by the NaS1 sulfate transporter which is expressed in the kidney. Previously, we generated a NaS1-null (Nas1(-/-)) mouse which exhibits hyposulfatemia. In this study, we investigated the kidney transcriptome of Nas1(-/-) mice. We found increased (n=25) and decreased (n=60) mRNA levels of genes with functional roles that include sulfate transport and steroid metabolism. Corticosteroid-binding globulin was the most up-regulated gene (110% increase) in Nas1(-/-) mouse kidney, whereas the sulfate anion transporter-1 (Sat1) was among the most down-regulated genes (>or=50% decrease). These findings led us to investigate the circulating and urinary steroid levels of Nas1(-/-) and Nas1(+/+) mice, which revealed reduced blood levels of corticosterone ( approximately 50% decrease), dehydroepiandrosterone (DHEA, approximately 30% decrease) and DHEA-sulfate ( approximately 40% decrease), and increased urinary corticosterone ( approximately 16-fold increase) and DHEA ( approximately 40% increase) levels in Nas1(-/-) mice. Our data suggest that NaS1 is essential for maintaining a normal metabolic state in the kidney and that loss of NaS1 function leads to reduced circulating steroid levels and increased urinary steroid excretion. |
