Hyperglycemia abolishes the protective effect of ischemic preconditioning in glomerular endothelial cells in vitro. Issue 3 (24th March 2015)

• Record Type: Journal Article
• Authors: Schenning, Katie J.; Anderson, Sharon; Alkayed, Nabil J.; Hutchens, Michael P.
• Is Part Of: Physiological reports. Volume 3:Issue 3(2015:Mar.)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2015-03-24
• Subjects: Glomerular endothelial cells -- hyperglycemia -- ischemic preconditioning -- renal ischemia–reperfusion injury; Physiology -- Periodicals; 571
• DOI: 10.14814/phy2.12346
• Languages: English
• ISSNs: 2051-817X

Abstract

Abstract: In preclinical investigations, ischemic preconditioning (IPC) protects kidneys from ischemia/reperfusion injury. The direct effects of IPC on glomerular endothelial cells have not been studied in detail. Most investigations of IPC have focused on healthy cells and animals, and it remains unknown whether IPC is renoprotective in the setting of medical comorbidities such as diabetes. In this study, we determined the preventive potential of IPC in healthy glomerular endothelial cell monolayers, and compared these results to monolayers cultured under hyperglycemic conditions. We exposed glomerular endothelial monolayers to 1 h of IPC 24 h prior to oxygen–glucose deprivation (OGD), an in vitro model of ischemia/reperfusion injury. Glomerular endothelial monolayer integrity was assessed by measuring transendothelial electrical resistance, albumin flux, and cell survival. We found that IPC protected healthy but not hyperglycemic glomerular endothelial monolayers from ischemia/reperfusion injury. Furthermore, not only was the protective effect of IPC lost in the setting of hyperglycemia, but IPC was actually deleterious to the integrity of hyperglycemic glomerular endothelial cell monolayers. Abstract : We exposed glomerular endothelial monolayers to an in vitro model of ischemia/reperfusion injury. We found that ischemic preconditioning protected healthy but not hyperglycemic glomerular endothelial monolayers from ischemia/reperfusion injury. Furthermore, not only was the protective effect of ischemic preconditioning lost in the setting of hyperglycemia, but ischemic preconditioning was actually deleterious to the integrity of hyperglycemic glomerular endothelial cell monolayers.