Disease relevance of Stc1

• Such a role is further supported by the presence of dwarfism in mice overexpressing STC1 [1].
• 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 (Pi) reabsorption [2].
• Here we show that the epithelium of the choroid plexus, already at 16 weeks of fetal age, and of plexus papillomas, synthesize and express STC [3].
• However, undifferentiated human adrenal neuroblastoma was negative for STC staining [4].

High impact information on Stc1

• Possible candidate genes for Stc1 and Rtc1 are discussed [5].
• DA rats had a semidominant gene (Stc1) favoring the development of 4-nitroquinoline 1-oxide-induced cancers on chromosome 19, closely linked to D19Mit9 [5].
• Stanniocalcin 1 acts as a paracrine regulator of growth plate chondrogenesis [1].
• Yet, the STC 1 inhibitory effect on growth may be related to both postnatal metabolic abnormalities and prenatal defective bone formation [1].
• Last, the expression of both STC1 and its binding site in the growth plate would support an autocrine/paracrine role for this growth factor in the regulation of growth plate chondrogenesis [1].

Chemical compound and disease context of Stc1

• Hypercalcemia increases STC secretion, which inhibits Ca uptake by the gills and normalizes serum Ca level [4].
• STC was also detected in human adrenal tumors, such as pheochromocytoma, differentiated neuroblastoma, and aldosterone-producing adenoma, and cultured adrenal tumor cells (rat pheochromocytoma PC-12 cells and human neuroblastoma NB-1 cells) [4].

Biological context of Stc1

• DA rats had a semidominant susceptibility gene, Stc1, closely linked with D19Mit9 on chromosome 19, which was on the segment syntenic to human chromosome 16 [6].
• We found that forskolin significantly increased STC gene expression and secretion by both rat and bovine TICs, an effect that was only replicated by human (h) chorionic gonadotropin (CG) [7].
• These results indicate that ovarian STC is physically distinct, a feature that could explain its presence in serum during pregnancy and lactation [7].
• Taken together, our findings indicate that STC1 inhibits longitudinal bone growth directly at the growth plate [1].
• During embryogenesis, the expression of mammalian stanniocalcin (STC1) in the appendicular skeleton suggests its involvement in the regulation of longitudinal bone growth [1].

Anatomical context of Stc1

• Thus, STC1 accelerates osteoblast development in an autocrine/paracrine manner in the RC cell culture model [8].
• Stanniocalcin 1 stimulates osteoblast differentiation in rat calvaria cell cultures [8].
• In two CCK-producing cell lines, RIN 1056E and STC-1 of pancreatic and intestinal origin respectively, dexamethasone induced dose-dependent decreases in both CCK-L1 and steady-state CCK mRNA levels [9].
• Expression of stanniocalcin in the epithelium of human choroid plexus [3].
• Our findings suggest that STC may be of importance for the distribution of calcium and phosphate between the cerebrospinal fluid and blood [3].

Associations of Stc1 with chemical compounds

• STC1 mRNA and protein were differentially expressed over the time course of cultures, and dexamethasone, a potent stimulator of differentiation in this model, shifted peak STC1 expression levels to earlier times [8].
• In rodents the STC gene is most highly expressed in ovary, specifically in androgen-producing thecal and interstitial cells [7].
• In the kidney, calcitriol treatment increased the STC-1 mRNA levels more than 3-fold, but decreased the STC-2 message to trace levels [10].
• Stanniocalcin (STC) is a glycoprotein hormone that was first discovered in fish and recently identified in mammals [11].
• In kidney, STC regulates phosphate reabsorption by proximal tubule cells, whereas in ovary it appears to be involved in steroid hormone synthesis [12].

Other interactions of Stc1

• Out of the five loci detected in this F2 generation, Tscc1 and 2 were identical to Stc1 and Rtc1 described in our previous study, but the other three were novel [13].
• We studied whether the above-mentioned neuropeptides can act directly on secretin-producing cells, including the murine neuroendocrine cell line STC-1 and a secretin cell-enriched preparation isolated from rat upper small intestinal mucosa [14].

Analytical, diagnostic and therapeutic context of Stc1

• Female rats were treated with calcitriol, the active form of vitamin D(3), and alterations in the levels of STC-1 and STC-2 mRNA were determined by Northern blot analysis in the kidney and ovary where the STC-1-expressing cells have previously been identified by in situ hybridization histochemistry [10].
• On the other hand, in situ hybridization revealed that the STC gene was expressed only in cortical and medullary collecting duct cells [11].
• In the present study we have identified STCir cells and tubules in the rat kidney by correlative immunocytochemistry using antibodies to STC and specific antigenic markers (Tamm-Horsfall protein and anion exchanger-1) [11].
• In this report we have developed a radioimmunoassay (RIA) for human STC [12].
• The current study employed Western blot analysis to characterize PTH and STC in neural tissues of high- (rats) and low- (hagfish, dogfish, rockfish, trout and skate) vertebrates and invertebrates (starfish, squid, cuttlefish, snails, prawns) [15].

References