Human Stanniocalcin Inhibits Renal Phosphate Excretion in the Rat

Abstract

Stanniocalcin (STC) is a glycoprotein hormone first identified in bony fishes where it counteracts hypercalcemia by inhibiting gill calcium uptake and stimulating renal inorganic phosphate (P i ) reabsorption. Human STC (hSTC) has recently been cloned and sequenced and is highly homologous to the fish hormone at the amino acid level. The objective of this study was to examine the possible effects of hSTC on electrolyte homeostasis and renal function in the rat. Recombinant hSTC was expressed in bacteria and purified by metal-ion affinity chromatography and reverse-phase high performance liquid chromatography. Anesthetized animals were given bolus infusions of 1, 5, or 10 nmol hSTC per kilogram of body weight. Control animals received solvent alone. The most effective dosage was 5 nmol/kg, which caused significant reductions in both absolute and fractional phosphate excretion in comparison with control rats. The hSTC had no effect on the renal excretion of other ions, the glomerular filtration rate, renal blood flow, blood pressure, or plasma electrolytes (Na

Stanniocalcin-1 as a Novel Marker to Detect Minimal Residual Disease of Human Leukemia

“…The sequence similarity of STC-1 to its fish counterparts suggests that human homologue, STC-1, regulates calcium and phosphate homeostasis in the kidney and intestine (Chang et al 1996a, b;Wagner et al 1997;Koide et al 1998;Madsen et al 1998;Varghese et al 1998). Human STC-1 mRNA is, however, expressed in multiple tissues, suggesting that human STC-1 might have additional functions, for example, neural cell differentiation (Zhang et al 1998), bone formation (Yoshiko et al 1998;Stasko et al 2001).…”

Synergistic effect of p53 on TSA-induced stanniocalcin 1 expression in human nasopharyngeal carcinoma cells, CNE2

“…Moreover, there is no solid evidence to illustrate that mammalian STC1 plays an important role in this aspect. With increasing evidence to demonstrate the local actions of STC1, the focus of STC1 research has been moved from serum Ca 2C /P i homeostasis to cellular inflammation and carcinogenesis (Wagner et al 1997, Madsen et al 1998, Chang et al 2003, Yoshiko & Aubin 2004, Ellard et al 2007, Re & Cook 2010, Sheikh-Hamad 2010.…”

Stanniocalcin-1 acts in a negative feedback loop in the prosurvival ERK1/2 signaling pathway during oxidative stress

“…In fish, it functions as a classic hormone that is secreted from endocrine glands, the Corpuscles of Stannius, in response to hypercalcemia and inhibits uptake of calcium through the gills and gut (Wagner et al, 1988;Sundell et al, 1992). In mammals, STC1 is also a secreted glycoprotein (Jellinek et al, 2000), but although recombinant human STC1 was found to be capable of inhibiting the uptake of calcium through the gills of goldfish (Olsen et al, 1996), and of regulating the flux of calcium and phosphate across rat intestine (Madsen et al, 1998) and kidney (Wagner et al, 1997), there is no evidence that it has a physiologic role in regulating serum calcium in mammals. Instead, mammalian STC1 is expressed in a variety of tissues (Chang et al, 1995(Chang et al, , 1996Olsen et al, 1996) and is thought to have an autocrine or paracrine role, but the possibility of an intracellular role also is suggested by evidence that STC1 localizes to mitochondria (McCudden et al, 2002;Westberg et al, 2007a).…”