Assistant Professor of Medicine, Division of Nephrology, Baylor College of Medicine, USA
Stanniocalcin-1 (STC1) is a glycoprotein hormone that is released by the corpuscle of stannous, an endocrine gland of bony fish; and upon circulation in the gills and intestine, it blocks calcium entry into the blood, thus maintaining a calcium concentration. Mammalian STC1 is ubiquitously expressed and the protein has been detected in many tissues including kidney, bone, brain, muscle, lung, and heart. While it circulates in the blood, it is believed to function as an intracrine substance. Recent studies in our lab have identified a novel role for mammalian STC1, namely, upregulation of mitochondrial uncoupling proteins and suppression of superoxide generation. STC1-mediated suppression of superoxide generation in macrophages inhibits macrophage function, while in endothelial cells STC-1 blocks cytokine-induced rise in cell permeability and the transmigration of lymphocytes and macrophages across activated (IL-1? or TNF?-treated) endothelial monolayer. In combination, these effects exert potent anti-inflammatory action. We applied ischemia/reperfusion kidney injury model or anti-GBM glomerulonephritis model to STC-1 transgenic mice that display preferential expression of STC-1 transgene in endothelial cells and macrophages.
On the basis of the previous findings, our current research interests include: first, to determine the protective roles and the underlying mechanisms of STC-1 in renal injury and inflammation by utilizing ultrasound microbubble-mediated gene delivery to the kidney in vivo; second, to investigate the role of STC-1 in ischemia/reperfusion kidney injury by utilizing STC-1 transgenic mice or STC-1 knock-out mice