¹College of Biological and Food Engineering, Huaihua University, Huaihua 418008, CHINA
²Key Laboratory of Research and Utilization of Ethnomedicinal Plant Resources of Hunan Province, Huaihua University, Huaihua 418008, CHINA DOI : 10.9775/kvfd.2024.32852 Stanniocalcin-1 (STC1), a glycoprotein, serves as an autocrine or paracrine factor in multiple processes in mammals, including the regulation of calcium/phosphorus (Ca2+/Pi) transport. However, its underlying mechanisms are not fully elucidated. Here, we examined the intracellular Ca2+ ([Ca²+]i) and Pi concentrations ([Pi]i) levels in primary bovine renal tubular epithelial cells (RTECs) using flow cytometry and phosphomolybdic spectrophotometry, respectively, following STC1 overexpression/ inhibition, and treatments with vitamin D3 receptor (VDR) agonist calcitriol or antagonist MeTC7. The expression of Ca2+/Pi transporters (TRPV5, TRPV6, CB-D28K, PMCA1b, NCX1, Npt2a, Npt2c) was measured by real-time qPCR and western blotting. The results revealed STC1 inhibition by STC1-shRNA promoted Ca2+ intake and inhibited Pi influx, whereas STC1 overexpression by pcDNA3.1/STC1 had the opposite effects. The calcitriol-induced increase in [Ca²+]i was reversed by STC1 overexpression and MeTC7 treatment. Overexpression of STC1 reduced the expression of TRPV5, TRPV6, and VDR, while suppressing calcitriol-induced TRPV5 upregulation and enhancing Npt2a/Npt2c expression. STC1 had no effect on CB-D28K, NCX1, or PMCA1b, which mediate Ca2+ diffusion and extrusion. In conclusion, our findings suggest STC1 inhibits Ca2+ transport and enhances Pi uptake in RTECs at least partly by regulating TRPV5/ TRPV6 and Npt2a/Npt2c expression, respectively. Interference of 1,25 (OH)2D3/VDR axis may also contribute. The present findings provide new insights into the underlying mechanisms of STC1 and offer strategies to prevent mineral disorders in cattle. Keywords : Ca2+/Pi transport, TRPV5/6, Npt2a/2c, RTECs, Stanniocalcin-1