| First Author | Tejada T | Year | 2008 |
| Journal | Kidney Int | Volume | 73 |
| Issue | 12 | Pages | 1385-93 |
| PubMed ID | 18385666 | Mgi Jnum | J:152875 |
| Mgi Id | MGI:4360164 | Doi | 10.1038/ki.2008.109 |
| Citation | Tejada T, et al. (2008) Failure to phosphorylate AKT in podocytes from mice with early diabetic nephropathy promotes cell death. Kidney Int 73(12):1385-93 |
| abstractText | Loss of podocytes by apoptosis characterizes the early stages of diabetic nephropathy. To examine its mechanism we studied glomeruli and podocytes isolated from db/db mice with early diabetic nephropathy and albuminuria. Phosphorylation of AKT (protein kinase B, a key survival protein) was found to be lower in the glomeruli of 12 week old db/db compared to db/+ mice. In vitro, insulin phosphorylated AKT solely in podocytes from db/+ mice. Serum deprivation and exposure to tumor necrosis factor-alpha significantly compromised cell viability in podocytes from db/db but not from db/+ mice, and this was associated with a significant decrease in AKT phosphorylation. Inhibition of AKT was necessary to achieve the same degree of cell death in db/+ podocytes. Our study shows that podocyte inability to respond to insulin and susceptibility to cell death may partially account for the decreased podocyte number seen in early diabetic nephropathy. |
