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Abstract: FR-PO710

Mesenchymal Stem Cells Acquire Phagocytotic Functions and Contractibility When They Repair Light Chain-Induced Mesangial Damage

Session Information

Category: Glomerular

  • 1002 Glomerular: Basic/Experimental Pathology


  • Zeng, Chun, LSUHSC-Shreveport, Shreveport, Louisiana, United States
  • Herrera, Guillermo A., LSUHSC-Shreveport, Shreveport, Louisiana, United States
  • Liang, Man, LSUHSC-Shreveport, Shreveport, Louisiana, United States
  • Xu, Hongzhi, LSUHSC-Shreveport, Shreveport, Louisiana, United States
  • Turbat-herrera, Elba, LSUHSC-Shreveport, Shreveport, Louisiana, United States
  • Teng, Jiamin, LSUHSC-Shreveport, Shreveport, Louisiana, United States

Using mesenchymal stem cells (MSCs) to repair the injured mesangium has been shown experimentally to be a promising approach. However, the precise role MSCs play in the repair process is still unclear. In this study, we investigated phagocytotic and contractibility capabilities of MSCs in the process of mesangial repair.


Mesangial cells (MCs) were incubated with AL-amyloidosis and light chain deposition disease G-LCs for 4 days to establish an in vitro mesangial cell injury model. Green fluorescent protein (GFP)-labeled MSCs were added together with florescent-labeled latex beads to assess phagocytotic activity of MSCs. A 6 dimensional (6D) live cell imaging system was used to record the process for 7 days after the introduction of the MSCs. Immunofluorescence, immunohistochemistry and electron microscopy were used to evaluate samples obtained at different time frames. Stains for smoothelin, CD68, CD29 and CD54 were used to monitor phenotypic expressions of MSCs. Collagen assay was used to evaluate contractibility.


MSCs migrated to the damaged mesangial areas and morphologically transformed from an undifferentiated to a macrophage phenotype. MSCs lost CD29/54 stem cell makers after G-LCs treatment, acquiring CD68, and later expressed smoothelin / muscle specific actin. Significant amount of the florescent-labeled latex beads were engulfed by transformed MSCs indicating active phagocytosis during the initial cleaning phase of the repair. MCs revealed decreased contractibility after G-LCs treatment while MSCs exhibited contractability during the late phase of the process, but not at the beginning of the repair. The plasticity of MSCs was confirmed ultrastructurally with findings of macrophage and smooth muscle differentiation at different stages of the repair process.


MSCs undergo both morphological and functional transformations as they proceed to repair the damaged mesangium. In contrast to previous belief that MSCs only enhance repair via a paracrine mechanism, this study provides evidence that MSCs differentiate sequentially from uncommitted to macrophage and finally smooth muscle (mesangial cell) phenotypes during the process of mesangial repair. This permits the repair process to replace the damaged mesangium with fully differentiated mesangial cells.