title: Sodium deficiency regulates rat adrenal zona glomerulosa gene expression.
abstract: 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.
authors.affiliation: Department of Molecular and Integrative Physiology (K.N., W.E.R.), University of Michigan, Ann Arbor, Michigan 48109; Department of Physiology (R.B.S.H., T.S.), Georgia Regents University, Augusta, Georgia 30912; and Department of Urology (K.N.), Tachikawa Hospital, Tachikawa, 190-0022 Tokyo, Japan.
authors.forename: Koshiro
authors.initials: K
authors.lastname: Nishimoto
authors.forename: Ruth B S
authors.initials: RB
authors.lastname: Harris
authors.forename: William E
authors.initials: WE
authors.lastname: Rainey
authors.forename: Tsugio
authors.initials: T
authors.lastname: Seki
mesh_terms: D000311:Adrenal Glands / Q000378:metabolism*; D000450:Aldosterone / Q000378:metabolism; D000818:Animals; D002784:Cholesterol / Q000737:chemistry; D004039:Diet, Sodium-Restricted; D005786:Gene Expression Regulation; D008297:Male; D020411:Oligonucleotide Array Sequence Analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000172:deficiency*; D017673:Sodium Chloride, Dietary; D013256:Steroids / Q000737:chemistry; D013997:Time Factors; D059467:Transcriptome; D015384:Zona Glomerulosa / Q000378:metabolism*
chemical_list: D017673:Sodium Chloride, Dietary; D013256:Steroids; D000450:Aldosterone; D002784:Cholesterol; D012964:Sodium