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Abstract: SA-PO094

Microparticles Released From Renal Epithelial Cells Induce Endothelial Cell Activation

Session Information

  • AKI: Mechanisms - III
    November 05, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Campos, Begoña, University of Cincinnati, Cincinnati, Ohio, United States
  • Shondel, Robert C., University of Cincinnati, Cincinnati, Ohio, United States
  • Bockhorst, Samuel Paul, University of Cincinnati, Cincinnati, Ohio, United States
  • Thakar, Charuhas V., University of Cincinnati, Cincinnati, Ohio, United States

Group or Team Name

  • College of Medicine, Division of Nephrology, Kidney C.A.R.E. Program. Kidney Injury Translational Laboratory.
Background

Acute kidney injury (AKI) is associated with an interplay between endothelium and epithelium as a part of both injury and repair cycles. We have shown that microparticles (MP) derived from renal epithelial cells are released in the setting of AKI and can carry the biological activity that could induce inflammation.

Methods

In this study, we evaluated if the MP derived from renal proximal tubular epithelial cells (RPTEC) after exposure to inflammatory stress-induced human umbilical vein endothelial cells (HUVEC) by using the monocyte adhesion assay. HUVEC and THP1 monocytes were maintained under standard cell culture conditions and exposed to RPTEC derived MP, TNFα, or vehicle (control). For Adhesion of THP1 cells to treated HUVEC, THP1 cells were labeled with Calcein Red Orange at a final concentration of 10 µmol/L. Total fluorescence intensity, automated THP1 cell counts, and fluorescence of blank media was measured with a Cytation 5 plate reader. Unbound THP1 cells were removed by washing, and the remaining fluorescence intensity and THP1 cell counts were measured again.

Results

Activation of endothelial cells is significantly greater in both RPTEC-derived MP activated (54.13 X 103) and direct activation from TNFα (42.90 X103) when compared with control (14.74X103) (p= 0.0002 and p=0.0047, respectively, Fig 1). Endothelial cell activation between RPTEC-derived MP vs. direct activation from TNFα was similar (p=0.1135).

Conclusion

MP derived from renal epithelial cells can induce endothelial cells as demonstrated by their ability to cause monocyte adhesion. These results suggest that microparticles can mediate cellular cross-talk, and in turn can affect injury and repair cycles in AKI.