Proteomics Data for "Streptozotocin induced diabetes augments expression of renal cell surface proteins and induces hypertension in cathepsin B knockout mice"

Cathepsin B (CtsB) plays a role in several biological processes in physiology and pathophysiology. Streptozotocin (STZ) treatment causes pancreatic beta cell distruction and type 1 diabetes in rodents. Here, we hypothesized STZ induces kidney damage, hypertension, and changes in expression of renal epithelial cell surface proteins independent of CtsB expression. In CtsB knockout mice, STZ treatment induced kidney damage, hypertension, and down-regulation of NPR-B and NPR-C protiens, presumably in part by causing a rearrangement of the actin cyctoskeleton in renal epithelial cells. These results suggest the expression of CtsB is not essential for the development of kidney damage, hypertension and reorganization of the actin cyctoskeleton in kidney.

组织蛋白酶B（Cathepsin B, CtsB）在生理与病理生理过程中参与多项生物学进程。链脲佐菌素（Streptozotocin, STZ）处理可诱导啮齿类动物胰岛β细胞破坏并诱发1型糖尿病。本研究假设，STZ可在不依赖CtsB表达的情况下，引发肾损伤、高血压，并改变肾上皮细胞表面蛋白的表达水平。在CtsB敲除小鼠中，STZ处理仍可诱导肾损伤、高血压，并下调利钠肽受体B（Natriuretic Peptide Receptor B, NPR-B）与利钠肽受体C（Natriuretic Peptide Receptor C, NPR-C）的蛋白表达，该过程可能部分通过介导肾上皮细胞的肌动蛋白细胞骨架（actin cytoskeleton）重排实现。上述结果表明，CtsB的表达对于肾损伤、高血压的发生以及肾组织肌动蛋白细胞骨架的重排并非必需。