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The Role of Par‐1a/b Polarity Proteins in Acute Kidney Injury

Acute Kidney Injury (AKI) is defined as the rapid loss of kidney function. Patients with acute kidney injury are unable to filter waste products from their body. The integrity of renal epithelial apico‐basal polarity is critical for many aspects of kidney function, including reabsorption of solutes. Loss of epithelial cell polarity occurs in several kidney disorders, including acute kidney injury. Partitioning defective 1 (Par‐1) is a member of the Par polarity protein family that localizes to the basolateral aspect of cells. Studies of Par‐1a+/−:Par‐1b−/− and Par‐1a−/−:Par‐1b+/− newborn mice determined that Par‐1 contributes to proximal tubular development. Complete loss of Par‐1a/b (Par‐1a−/−: Par‐1b−/−) leads to death early in fetal development of mice. Par‐1a and Par‐1b are expressed in developing nephrons and their expression decreases in adult nephrons. Tubular injury in mice correlates with increased expression of Par‐1a and Par‐1b. In our research, we hypothesized that Par‐1a/b polarity proteins are protective in the setting of acute kidney injury. In order to test this, cisplatin was injected intraperitoneal into Par‐1a/b global knockout mice at 5 weeks and they were sacrificed 3 days after injection. Cisplatin is one of the most widely used chemotherapy drugs that has been recently found to contribute to nephrotoxicity, especially on the signaling pathways leading to renal tubular cell death and inflammation. Hematoxylin and Eosin (H&E) staining was performed to assess tubular injury. Controls were non‐injected Par‐1a−/− and Par‐1b−/− mutants and injected wild type littermates. Ki‐67 staining was performed to identify cell proliferation. The level of tubular injury and cellular proliferation was examined by light microscopy. Our data showed that Par‐1b knockout mice were more susceptible to renal tubular injury than controls. Par‐1b knockout mice also had decreased cellular proliferation after cisplatin injury. Our ongoing experiment is testing the role of Par‐1a in AKI. In conclusion, Par‐1b polarity proteins contribute to renal tubular epithelial response to injury. Either decreased or delayed cellular proliferation may contribute to the increased tubular injury in Par‐1b−/− mice.