Bmi-1 plays a critical role in the protection from acute tubular necrosis by mobilizing renal stem/progenitor cells

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• 作者：Xianhui Lv^a ; Zhenzhen Yu^a ; Chunfeng Xie^a ; Xiuliang Dai^a ; Qing Li^b ; Dengshun Miao^a ; Jianliang Jin^a ; ^{jinjianliang@njmu.edu.cn}
• 关键词：Bmi-1 ; Acute tubular necrosis ; Renal stem/progenitor cells ; Mobilization ; Rhabdomyolysis-induced renal failure
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2017
• 出版时间：22 January 2017
• 年：2017
• 卷：482
• 期：4
• 页码：742-749
• 全文大小：5376 K
• 卷排序：482

文摘

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.