| Autor: |
Meyer MH; Orthopaedic Research Laboratory, Carolinas Medical Center, Charlotte, North Carolina 28232-2861, USA., Dulde E, Meyer RA Jr |
| Jazyk: |
angličtina |
| Zdroj: |
Physiological genomics [Physiol Genomics] 2004 Jun 17; Vol. 18 (1), pp. 4-11. Date of Electronic Publication: 2004 Jun 17. |
| DOI: |
10.1152/physiolgenomics.00210.2003 |
| Abstrakt: |
The mechanism for the renal adaptation to low-phosphate diets is not well understood. Whether the Hyp mutation of the Phex gene blocks this adaptation is also not clear. To gain further insight into this, 5-wk-old normal and Hyp mice were fed a control (1.0% P) or low-phosphate diet (0.03% P) for 3-5 days. Renal RNA was hybridized to Affymetrix U74Av2 microarrays (5 arrays/group). Of the 5,719 detectable genes on each array, 290 responded significantly (P < 0.01) to low-phosphate diet in normal mice. This was reduced significantly (P < 0.001) to 7 in the Hyp mice. This suggested that the adaptations of the normal kidney to a low-phosphate environment were blocked by the Hyp mutation. The Npt2 phosphate transporter, vitamin D 1alpha- and 24-hydroxylases, and calbindins D9K and D28K responded in the expected fashion. Genes with significant (P < 0.05) diet-by-genotype interaction were analyzed by GenMAPP and MAPPFinder. This revealed a cluster of differentially expressed genes associated with microtubule-based processes. Most alpha- and beta-tubulins and most kinesins had responses to low-phosphate diet in normal mice which were abolished or reversed in Hyp mice. In summary, renal adaptation to low-phosphate diet involved changes in the mRNA expression of specific genes. Disruption of these responses in Hyp mice may contribute to their abnormal phosphate homeostasis. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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