Cyclooxygenase-2 mediates induction of the renal stanniocalcin-1 gene by arginine vasopressin.

In rats and mice, the renal stanniocalcin-1 (STC-1) gene is expressed in most nephron segments, but is differentially induced in response to dehydration. In cortical segments STC-1 mRNA levels are upregulated by the hypertonicity of dehydration, while hypovolemia causes gene induction in the inner medulla (papilla). In both cases induction is mediated by arginine vasopressin (AVP) acting via the V2 receptor (V2R).

Stanniocalcin-1 co-localizes with insulin in the pancreatic islets.

The polypeptide hormone stanniocalcin-1 (STC-1) is widely expressed in mammals and signals both locally and systemically. In many tissues STC-1 ligand is sequestered by target cell organelles (mitochondria, nuclei, and cholesterol lipid droplets) to exert diverse biological effects. Most notably, STC-1 serves as an uncoupler of oxidative phosphorylation in liver, muscle, and kidney mitochondria.

Stanniocalcin-1 in the subfornical organ inhibits the dipsogenic response to angiotensin II.

Recently, receptors for the calcium-regulating glycoprotein hormone stanniocalcin-1 (STC-1) have been found within subfornical organ (SFO), a central structure involved in the regulation of electrolyte and body fluid homeostasis. However, whether SFO neurons produce STC-1 and how STC-1 may function in fluid homeostasis are not known. Two series of experiments were done in Sprague-Dawley rats to investigate whether STC-1 is expressed within SFO and whether it exerts an effect on water intake.

Characterization of stanniocalcin-1 receptors in the rainbow trout.

Mammalian stanniocalcin-1 (STC-1) is one of several ligands targeted to mitochondria. High affinity STC-1 receptors are present on the mitochondrial membranes of nephron cells, myocytes, and hepatocytes, to enable ligand sequestration within the matrix. However, STC-1 receptors have not been characterized in fish.

Vasopressin controls stanniocalcin-1 gene expression in rat and mouse kidney.

Renal stanniocalcin-1 (STC-1) is made by collecting duct principal cells for autocrine and paracrine targeting of the distal nephron. While the underlying purpose of this targeting is poorly understood, increased targeting is tied to changes in extracellular fluid (ECF) balance. For example, water deprivation is a potent stimulator of renal STC-1 gene activity in both rats and mice.

The renal stanniocalcin-1 gene is differentially regulated by hypertonicity and hypovolemia in the rat.

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.

Induction of the renal stanniocalcin-1 gene in rodents by water deprivation.

Stanniocalcin-1 (STC-1) is made by kidney collecting duct cells for targeting of nephron mitochondria to promote respiratory uncoupling and calcium uniport activity. However, the purpose of these actions and how the renal gene is regulated are poorly understood. This study has addressed the latter issue by monitoring renal STC-1 gene expression in different models of kidney function.

The corpuscles of Stannius, calcium-sensing receptor, and stanniocalcin: responses to calcimimetics and physiological challenges.

This study has examined whether the calcium-sensing receptor (CaSR) plays a role in control of stanniocalcin-1 (STC-1), the dominant calcium regulatory hormone of fish, comparable with that demonstrated for CaSR in the mediation of ionized calcium regulation of PTH secretion in mammals. In a previous study, we have cloned flounder STC-1 from the corpuscles of Stannius (CS). Here, we report the cloning and characterization of the CS CaSR, and the in vivo responses of this system to altered salinity, EGTA induced hypocalcemia, and calcimimetic administration.

Stanniocalcin 1 is a luminal epithelial marker for implantation in pigs regulated by progesterone and estradiol.

Stanniocalcin 1 (STC1) is a glycoprotein that decreases calcium and increases phosphate in cells/tissues. This investigation examined endocrine regulation of STC1 in endometria of pigs during the estrous cycle and pregnancy. STC1 mRNA was present exclusively in luminal epithelium (LE) between d 12 and 15 of the estrous cycle, increased between d 12 and d 20, and was not detectable by d 30 of pregnancy.

Distribution of stanniocalcin binding sites in the lamina terminalis of the rat.

Stanniocalcin (STC-1), a 50 kDa glycoprotein hormone that regulates calcium/phosphate homeostasis in bony fish and mammals, has been shown to be expressed in central neurons and choroid plexus, and to exert a protective effect against hypercalcemic and hypoxic damage to neurons. Circumventricular organs are known to function in the regulation of ion and body fluid balance. Therefore, the possibility exists that STC-1 may be involved in the regulation of calcium/phosphate and fluid homeostasis through its actions on these central sites.

Epigenetic and HIF-1 regulation of stanniocalcin-2 expression in human cancer cells.

Mammalian stanniocalcin-2 (STC2) is a secreted glycoprotein hormone with a putative role in unfolded protein response and apoptosis. Here we reported that STC2 expression was sporadically abrogated in human cancer cells by transcriptional silencing associated with CpG island promoter hypermethylation. Direct sequencing of bisulfite-modified DNA from a panel of seven human cancer cell lines revealed that CpG dinucleotides in STC2 promoter was methylated in human ovarian epithelial cancer (SKOV3, OVCAR3 and CaOV3), pancreatic cancer (BxP3), colon adenoma (HT29), and leukemia (Jurkat cells).

Stanniocalcin-1 secretion and receptor regulation in kidney cells.

Kidney collecting duct principal cells are the main source of stanniocalcin-1 (STC-1) production and secretion. From there, the hormone targets thick ascending limb and distal convoluted tubule cells, as well as collecting duct cells. More specifically, STC-1 targets their mitochondria to exert putative antiapoptotic effects.

Induction of stanniocalcin-1 expression in apoptotic human nasopharyngeal cancer cells by p53.

There is growing evidence to suggest that altered patterns of STC1 gene expression relate to the process of human cancer development. Our previous study has demonstrated the involvement of HIF-1 in the regulation of STC1 expression in human cancer cells. Recently, STC1 has been implicated as a putative pro-apoptotic factor in regulating the cell-death mechanism.

The respiratory effects of stanniocalcin-1 (STC-1) on intact mitochondria and cells: STC-1 uncouples oxidative phosphorylation and its actions are modulated by nucleotide triphosphates.

Stanniocalcin-1 (STC-1) is one of only a handful of hormones that are targeted to mitochondria. High affinity receptors for STC-1 are present on cytoplasmic membranes and both the outer and inner mitochondrial membranes of nephron cells and hepatocytes. In both cell types, STC-1 is also present within the mitochondrial matrix and receptors presumably enable its sequestration.

The stanniocalcin family of proteins.

Stannniocalcin (STC) is a polypeptide hormone that was originally identified in bony fishes as a systemic regulator of mineral metabolism, and is best known for its regulatory effects on calcium/phosphate transport by the gills, gut and kidneys. The mammalian homolog to fish STC was discovered in 1995 and has resulted in progressively growing interest ever since as to its possible role in humans. Moreover, new discoveries in the mammalian STC field are resulting in significant reappraisals as to its role in fishes.

Passive immunization of lactating mice with stanniocalcin-1 antiserum reduces mammary gland development, milk fat content, and postnatal pup growth.

During pregnancy and lactation in rodents, stanniocalcin-1 (STC-1) production by the ovaries is upregulated markedly and released into the circulation. The mammary glands are one target of this systemically delivered hormone. The purpose of this study was to lower serum levels of STC-1 in lactating mice through passive immunization so as to monitor the effects on mammary gland function and postnatal pup growth.

Stanniocalcin (STC) in the endometrial glands of the ovine uterus: regulation by progesterone and placental hormones.

Stanniocalcin (STC) is a hormone in fish that regulates calcium levels. Mammals have two orthologs of STC with roles in calcium and phosphate metabolism and perhaps cell differentiation. In the kidney and gut, STC regulates calcium and phosphate homeostasis.

Evidence for cross-talk between stanniocalcins.

There are 2 forms of stanniocalcin (STC) produced by the STC-1 gene; a 50 kDa polypeptide known as STC50 and a recently discovered group of higher molecular weight variants that are collectively referred to as big STC. Both have different tissue patterns of expression and different intracellular targeting pathways. STC50 functions locally in tissues such as muscle, liver, and kidney and is targeted to mitochondria.

Nuclear targeting of stanniocalcin to mammary gland alveolar cells during pregnancy and lactation.

In most mammalian tissues, the stanniocalcin-1 gene (STC-1) produces a 50-kDa polypeptide hormone known as STC50. Within the ovaries, however, the STC-1 gene generates three higher-molecular-mass variants known as big STC. Big STC is targeted locally to corpus luteal cells to block progesterone release.

Hypoxia-inducible factor-1-mediated activation of stanniocalcin-1 in human cancer cells.

Stanniocalcin-1 (STC1) is an endocrine hormone originally discovered in the corpuscles of Stannius, endocrine glands on kidneys of bony fishes, and also has been identified in mammals. The mammalian STC1 gene is widely expressed in various tissues and appears to be involved in diverse biological processes. There is growing evidence to suggest that altered patterns of gene expression have a role in human cancer development.

Characterization of big stanniocalcin variants in mammalian adipocytes and adrenocortical cells.

The hormone stanniocalcin (STC) is widely distributed, and in rodents the highest levels of expression are in the ovaries. In both cows and rodents, ovarian STC consists of three high-molecular-weight variants collectively known as big STC. In the ovary, big STC is made by theca cells and interstitial cells and is targeted to lipid storage droplets of nearby luteal cells to inhibit progesterone release.

Stanniocalcin: no longer just a fish tale.

Stanniocalcin was originally described as a hormone with calcitonin-like actions in fish. During the last decade, mammalian forms of stanniocalcin have been identified, and this discovery has led to important advances in our understanding of this enigmatic polypeptide hormone. This review briefly covers some early studies on stanniocalcin in fish and then provides a more in-depth look at some of the more intriguing, new aspects of its functions in mammals.

Evidence for stanniocalcin binding activity in mammalian blood and glomerular filtrate.

Background: The 50 kD form of the hormone stanniocalcin-1 (STC50) is widely distributed in organs such as kidney, lung, and liver. Kidney collecting duct cells produce STC50 for local targeting to proximal tubule cells to increase phosphate reabsorption. As such the current dogma is that in most organs STC50 is a purely local mediator that is not released into the circulation.

Evidence for stanniocalcin and a related receptor in annelids.

Stanniocalcin (STC) is a prime example of a hormone whose discovery in fish led to its subsequent discovery in mammals. STC is considered to be first and foremost a vertebrate polypeptide hormone with regulatory effects on ion transport, mitochondrial function and steroid hormone synthesis. The gene is widely expressed in both fishes and mammals, and the hormone can operate via both local and endocrine signaling pathways.

Human stanniocalcin-2 exhibits potent growth-suppressive properties in transgenic mice independently of growth hormone and IGFs.

Stanniocalcin (STC)-2 was discovered by its primary amino acid sequence identity to the hormone STC-1. The function of STC-2 has not been examined; thus we generated two lines of transgenic mice overexpressing human (h)STC-2 to gain insight into its potential functions through identification of overt phenotypes. Analysis of mouse Stc2 gene expression indicates that, unlike Stc1, it is not highly expressed during development but exhibits overlapping expression with Stc1 in adult mice, with heart and skeletal muscle exhibiting highest steady-state levels of Stc2 mRNA.