ArticleScientific reports2019
Premobilization of CD133+ cells by granulocyte colony- stimulating factor attenuates ischemic acute kidney injury induced by cardiopulmonary bypass.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 3 citations in OpenAlex.
- PAX2 induces endometrial cancer by inhibiting mitochondrial function via the CD133-AKT1 pathway.Molecular and cellular biochemistry · 2025Article
- Transcriptome Analysis of Kidney Grafts Subjected to Normothermic Ex Vivo Perfusion Demonstrates an Enrichment of Mitochondrial Metabolism Genes.Transplantation direct · 2021Article
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5 authors at 1 institution in 1 country.
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Abstract
Ischemic acute kidney injury (IAKI) is a common but severe complication after a cardiopulmonary bypass (CPB). Multiple studies have demonstrated that peripheral CD133+ or differentiated cells are able to home and repair the damaged tissues, but the number of available CD133+ cells is limited, and no efficient method published previously to mobilize them immediately. We analyzed the relationship between CD133+ cells and renal function in CPB patients, in addition, the efficacy of granulocyte colony-stimulating factor (G-CSF) pre-mobilized CD133+ cells in treating of mouse IAKI model have been investigated. In the clinical study, the prospective cohort study analyzed the correlation between BUN/Crea level and the peripheral CD133+ cell numbers. CPB was associated with postoperative renal dysfunction. The significant negative correlation was observed between patients' Crea and CD133+ cells (P < 0.05). The proposed mechanism studies were performed on the mouse IAKI model. The experimental mice were treated by G-CSF to mobilize CD133+ cells before implementing CPB. Data on cell count, inflammatory index, renal function/injury, and CD133+ cell mobilization were analyzed. The result demonstrated that pretreatment by G-CSF resulted in tremendous increase in the number of mouse peripheral blood and renal CD133+ cells, significantly reduces renal tissue inflammation and dramatically improves the renal function after CPB. In summary, we concluded that premobilization of CD133+ cells abated CPB induced IAKI, by promoting both repairing damaged epithelium and by its anti-inflammatory activity. Our findings stress the remarkable applications of CD133+ or differentiated cells-based therapies for potential preventing ischemic acute kidney injury.
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