| First Author | Jin X | Year | 2013 |
| Journal | Kidney Int | Volume | 83 |
| Issue | 4 | Pages | 604-14 |
| PubMed ID | 23302722 | Mgi Jnum | J:202445 |
| Mgi Id | MGI:5519030 | Doi | 10.1038/ki.2012.408 |
| Citation | Jin X, et al. (2013) Genetic deficiency of adiponectin protects against acute kidney injury. Kidney Int 83(4):604-14 |
| abstractText | Adiponectin is a multifunctional cytokine that has a role in regulating inflammation. Here we determined whether adiponectin modulates ischemic acute kidney injury. Compared with wild-type mice, adiponectin-knockout mice were found to have lower serum creatinine and less tubular damage or apoptosis following ischemia/reperfusion injury. This latter process was associated with decreased Bax and reduced activation of p53 and caspase-3. Targeted disruption of adiponectin was also found to inhibit the infiltration of neutrophils, macrophages, and T cells into the injured kidneys. This was associated with inhibition of NF-kappaB activation and reduced expression of the proinflammatory molecules IL-6, TNF-alpha, MCP-1, and MIP-2 in the kidney after ischemia/reperfusion injury. Wild-type mice engrafted with adiponectin-null bone marrow had less kidney dysfunction and tubular damage than adiponectin-null mice engrafted with wild-type bone marrow. Conversely, adiponectin-null mice engrafted with wild-type bone marrow had similar renal dysfunction and tubular damage compared with wild-type mice engrafted with wild-type bone marrow. In cultured macrophages, adiponectin directly promoted macrophage migration: a process blocked by the PI3 kinase inhibitor, LY294002. Thus, our results show that adiponectin has a pivotal role in the pathogenesis of acute renal ischemia/reperfusion injury and may be a potential therapeutic target. |
