Abstract
Renal ischemia/reperfusion is a major cause of acute kidney injury. However, the pathogenic mechanisms underlying renal ischemia/reperfusion injury (IRI) are not fully defined. Here, we investigated the role of PTEN, a dual protein/lipid phosphatase, in the development of ischemic AKI in mice. Pharmacological inhibition of PTEN with bpV(HOpic) exacerbated renal dysfunction and promoted tubular damage in mice with IRI compared with vehicle-treated mice with IRI. PTEN inhibition enhanced tubular cell apoptosis in kidneys with IRI, which was associated with excessive caspase-3 activation. Furthermore, PTEN inhibition expanded the infiltration of neutrophils and macrophages into kidneys with IRI, which was accompanied by increased expression of the proinflammatory molecules. These results have demonstrated that PTEN plays a crucial role in the pathogenesis of ischemic acute kidney injury through regulating tubular cell apoptosis and inflammation suggesting PTEN could be a potential therapeutic target for acute kidney injury.