title: The renal stanniocalcin-1 gene is differentially regulated by hypertonicity and hypovolemia in the rat.
abstract: Stanniocalcin-1 (STC-1) is made by kidney collecting duct cells for autocrine and paracrine targeting of nephron cell mitochondria. Here, the ligand stimulates respiratory uncoupling and calcium uniport activity. However, the underlying purpose of these actions and how the renal gene is regulated are poorly understood. In a previous study, we described the time-dependent, stimulatory effects of water deprivation on renal STC-1 mRNA levels in both rats and mice. In cortical kidney, STC-1 mRNA levels were increased 8-fold by 72h of water deprivation, whereas the gene response in outer and inner medulla was less pronounced (2-4 fold). Gene induction occurred equally in males and females and was accompanied by increased mitochondrial STC-1 protein levels. As water deprivation increases extracellular fluid (ECF) tonicity and at the same time reduces ECF volume, the present study examined the individual effects of hypertonicity and hypovolemia on renal gene activity in rats. Hypertonicity, whether induced by mannitol, glucose or NaCl, uniquely stimulated the cortical gene, to the extent that transcript levels were positively correlated with serum osmolality. This was in contrast to high dietary sodium, which had no bearing on cortical or medullary transcript levels. The situation was reversed in the case of hypovolemia. Inner medullary gene expression was uniquely induced by hypovolemia (low sodium diet or polyethylene glycol) such that transcript levels were positively correlated with hematocrit, while cortical gene activity was unaffected or reduced. Hence, the cortical and medullary genes proved to be differentially regulated by changing ECF tonicity and volume, respectively. The findings are therefore indicative of cortical and medullary STC-1 having separate roles in the renal control of ECF balance.
authors.affiliation: Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON, Canada.
authors.forename: Jeffrey
authors.initials: J
authors.lastname: Turner
authors.forename: Fu-Li
authors.initials: FL
authors.lastname: Xiang
authors.forename: Qingping
authors.initials: Q
authors.lastname: Feng
authors.forename: Graham F
authors.initials: GF
authors.lastname: Wagner
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D005260:Female; D005786:Gene Expression Regulation / Q000187:drug effects*; D006023:Glycoproteins / Q000235:genetics* / Q000378:metabolism; D006400:Hematocrit; D006982:Hypertonic Solutions / Q000494:pharmacology*; D020896:Hypovolemia / Q000235:genetics* / Q000503:physiopathology; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism* / Q000503:physiopathology; D007672:Kidney Cortex / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D007679:Kidney Medulla / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D051379:Mice; D009994:Osmolar Concentration; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012965:Sodium Chloride / Q000494:pharmacology; D013997:Time Factors
chemical_list: D001786:Blood Glucose; D006023:Glycoproteins; D006982:Hypertonic Solutions; D012333:RNA, Messenger; D012965:Sodium Chloride; C051795:teleocalcin