Overexpression of Soluble Fibrinogen-like Protein 2 in MSCs Ameliorates Renal Ischemia-Reperfusion Injury in Mice by Modulating Neutrophils

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Background Renal ischemia-reperfusion (I/R) injury is a major cause of graft dysfunction and failure, driving inflammation and tissue damage. Mesenchymal stem cells (MSCs) possess therapeutic potential due to their immunomodulatory properties. Notably, neutrophils express the inhibitory receptor CD32b, which is a specific target of the immunosuppressive molecule soluble fibrinogen-like protein 2 (sFgl2). Aims To investigate the therapeutic efficacy and underlying mechanisms of genetically engineered MSCs expressing sFgl2 (sFgl2-MSCs) in treating renal I/R injury, with a focus on neutrophil regulation. Study design An in vivo renal I/R injury mouse model. Methods Following imaging to localize MSCs, mice were randomly allocated into four treatment groups. Treatments were administered according to group assignments. Renal function was assessed using serum creatinine and blood urea nitrogen levels, while systemic inflammation was evaluated by measuring serum interleukin-1 beta (IL-1β), IL-6, tumor necrosis factor-alpha (TNF-α), and IL-10 via enzyme-linked immunosorbent assay (ELISA). Neutrophil proportions in the blood and kidney were analyzed by flow cytometry. At 24 h, surface expression of CD95 and CD206 was assessed; CD206 was used to define neutrophils with N2-like (CD206 + ) and N1-like (CD95 + ) phenotypic features. Histopathological scoring of renal tissue was performed at

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.