In:
Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 98, No. 5 ( 2001-02-27), p. 2712-2716
Kurzfassung:
Aldosterone and vasopressin are responsible for the final
adjustment of sodium and water reabsorption in the kidney. In principal cells of the kidney cortical collecting duct (CCD), the integral
response to aldosterone and the long-term functional effects of vasopressin depend on transcription. In this study, we analyzed the
transcriptome of a highly differentiated mouse clonal CCD principal cell line (mpkCCD cl4 ) and the changes in the transcriptome
induced by aldosterone and vasopressin. Serial analysis of gene expression (SAGE) was performed on untreated cells and on cells treated
with either aldosterone or vasopressin for 4 h. The transcriptomes in these three experimental conditions were determined by sequencing
169,721 transcript tags from the corresponding SAGE libraries. Limiting the analysis to tags that occurred twice or more in the data set,
14,654 different transcripts were identified, 3,642 of which do not match known mouse sequences. Statistical comparison (at P 〈 0.05 level) of the three SAGE libraries
revealed 34 AITs (aldosterone-induced transcripts), 29 ARTs (aldosterone-repressed transcripts), 48 VITs (vasopressin-induced
transcripts) and 11 VRTs (vasopressin-repressed transcripts). A selection of the differentially-expressed, hormone-specific transcripts
(5 VITs, 2 AITs and 1 ART) has been validated in the mpkCCD cl4 cell line either by Northern blot hybridization
or reverse transcription–PCR . The hepatocyte nuclear
transcription factor HNF-3-α (VIT39), the receptor activity modifying protein RAMP3 (VIT48), and the glucocorticoid-induced leucine zipper
protein (GILZ) (AIT28) are candidate proteins playing a role in physiological responses of this cell line to vasopressin and
aldosterone.
Materialart:
Online-Ressource
ISSN:
0027-8424
,
1091-6490
DOI:
10.1073/pnas.051603198
Sprache:
Englisch
Verlag:
Proceedings of the National Academy of Sciences
Publikationsdatum:
2001
ZDB Id:
209104-5
ZDB Id:
1461794-8
SSG:
11
SSG:
12
