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Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Endocrinology 2014 ; 155 (4): 1363-72 Nephropedia Template TP
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Sodium Deficiency Regulates Rat Adrenal Zona Glomerulosa Gene Expression #MMPMID24422541
Nishimoto K; Harris RBS; Rainey WE; Seki T
Endocrinology 2014[Apr]; 155 (4): 1363-72 PMID24422541show ga
Aldosterone is the primary adrenocortical hormone regulating sodium retention, and its production is under the control of the renin-angiotensin-aldosterone system (RAAS). In vitro, angiotensin II can induce aldosterone production in adrenocortical cells without causing cell proliferation. In vivo, a low-sodium diet activates the RAAS and aldosterone production, at least in part, through an expansion of the adrenal zona glomerulosa (zG) layer. Although these mechanisms have been investigated, RAAS effects on zG gene expression have not been fully elucidated. In this study, we took an unbiased approach to define the complete list of zG transcripts involved in RAAS activation. Adrenal glands were collected from 11-week old Sprague-Dawley rats fed either sodium-deficient (SDef), normal sodium (NS), or high-sodium (HS) diet for 72 hours, and laser-captured zG RNA was analyzed on microarrays containing 27 342 probe sets. When the SDef transcriptome was compared with NS transcriptome (SDef/NS comparison), only 79 and 10 probe sets were found to be up- and down-regulated more than two-fold in SDef, respectively. In SDef/HS comparison, 201 and 68 probe sets were up- and down-regulated in SDef, respectively. Upon gene ontology (GO) analysis of these gene sets, we identified three groups of functionally related GO terms: cell proliferation-associated (group 1), response to stimulus-associated (group 2), and cholesterol/steroid metabolism-associated (group 3) GO terms. Although genes in group 1 may play a critical role in zG layer expansion, those in groups 2 and 3 may have important functions in aldosterone production, and further investigations on these genes are warranted.
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Endocrinology 2014 ; 155 (4): 1363-72
