| First Author | Liang S | Year | 2015 |
| Journal | Mol Immunol | Volume | 65 |
| Issue | 2 | Pages | 321-7 |
| PubMed ID | 25728641 | Mgi Jnum | J:231555 |
| Mgi Id | MGI:5771745 | Doi | 10.1016/j.molimm.2015.02.003 |
| Citation | Liang S, et al. (2015) MicroRNA 26a modulates regulatory T cells expansion and attenuates renal ischemia-reperfusion injury. Mol Immunol 65(2):321-7 |
| abstractText | Ischemia-reperfusion injury (IRI) was one of the main causes of acute kidney injury. Mir-26a has been reported to play functions in cellular differentiation, cell growth, cell apoptosis and metastasis. Furthermore, the renal vein levels of Mir-26a were demonstrated to be lower in the poststenotic kidney. However, the effect of Mir-26a on the renal IRI has never been investigated. In our current study, Mir-26a overexpression results in attenuated renal IRI and promoted tregs expansion. The promoted renal function after IRI induced by Mir-26a overexpression was abrogated by depletion of tregs with anti-CD25 antibodies. Mir-26a also significantly suppressed IL-6 expression. And IL-6 overexpression led to significant suppression of the Mir-26a-induced upregulation of Foxp3. Next, we performed additional experiments to determine the therapeutic potential of Mir-26a during the recovery phase after renal IRI. Results showed that Mir-26a treatment after IRI also induced significant expansion of Foxp3(+)CD4(+) Tregs in both spleen and renal on day 10 after IRI. Taken together, our data indicate an important role for Mir-26a in promoting tregs expansion in renal IRI that involving repression of IL-6 expression. |
