| First Author | Lv X | Year | 2017 |
| Journal | Biochem Biophys Res Commun | Volume | 482 |
| Issue | 4 | Pages | 742-749 |
| PubMed ID | 27871857 | Mgi Jnum | J:241245 |
| Mgi Id | MGI:5898191 | Doi | 10.1016/j.bbrc.2016.11.105 |
| Citation | Lv X, et al. (2017) Bmi-1 plays a critical role in the protection from acute tubular necrosis by mobilizing renal stem/progenitor cells. Biochem Biophys Res Commun 482(4):742-749 |
| abstractText | The regeneration of injured tubular cell occurs primarily from intrinsic renal stem/progenitor cells (RSCs) labeled with CD24 and CD133 after acute tubular necrosis (ATN). Bmi-1 plays a crucial role in regulating self-renewal, differentiation and aging of multiple adult stem cells and progenitor cells. Bmi-1 was rapidly elevated in the induction of adult kidney regeneration by renal injury. To determine whether Bmi-1 maintained mobilization of RSCs in the protection from ATN, glycerol-rhabdomyolysis-induced ATN were performed in wild type (WT) and Bmi-1-deficient (Bmi-1-/-) mice. Their ATN phenotypes were analyzed; CD24 and CD133 double positive (CD24+CD133+) cells were measured; and the levels of serum urea nitrogen (SUN) and serum creatinine (SCr) were detected. We found that CD24+CD133+ RSCs were mobilized in WT ATN mice with the increased expression of Bmi-1; Bmi-1 deficiency led to increased tubular cast formation and necrosis, elevated levels of SUN and SCr, decreased tubular proliferation, and immobilized ratio of RSCs in ATN. These findings indicated that Bmi-1 played a critical role in the protection from ATN by maintaining mobilization of RSCs and would be a novel therapeutic target for preventing the progression of ATN. |
