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Abstract: TH-PO255

Thrombospondin-1 (TSP-1) and Microparticles in AKI

Session Information

Category: Acute Kidney Injury

  • 001 AKI: Basic


  • Campos, Begoña, University of Cincinnati, Cincinnati, Ohio, United States
  • Gleich, Brittany N, University of Cincinnati, Cincinnati, Ohio, United States
  • Singh, Sonam S, University of Cincinnati, Cincinnati, Ohio, United States
  • Domenico, Karen M, Shriners Hospitals for Children, Cincinnati, Ohio, United States
  • Thakar, Charuhas V., University of Cincinnati, Cincinnati, Ohio, United States

We have previously shown (Thakar et al, JCI, 2005) that TSP-1 is up-regulated and mediates kidney damage (AKI) in murine ischemia reperfusion injury. TSP-1 exposure to renal epithelial cells is also known to induce apoptosis/necrosis. TSP-1 exerts its inflammatory modulating effects through signaling of CD36 (pro-inflammatory) and CD47 (anti-inflammatory) ligands. Microparticles (MP's) are released in response to stress or injury from various cells and can serve as markers of type and state of cell activation. Whether TSP-1 induced inflammatory ligands can be detected as MP's, and could play a role in organ cross-talk in models of AKI is unknown.


By studying in vitro models of AKI using immortalized human renal proximal tubular epithelial cell (RPTEC) line, we incubated cells with and without TSP-1 (1 μg/ml for 24 hours) (N = 3 sets). MP's were isolated and evaluated by flow cytometry techniques and with CD36 and CD47 flourescent antibodies. Analyses of microparticles was performed using flow-jo software and levels of MP's was expressed as mean and standard deviation times 105. Unpaired t-tests were used for comparison.


Morphological assessment of TSP-1 treated cells confirmed characteristics assocaited with apoptosis. CD36 MP’s were significnatly higher in TSP-1 treated cells vs controls (92.66 +/- 11.06 vs 229 +/-69.77; p = 0.007). CD47 MP’s were statistically similar in TSP-1 and control cells (715.33 +/- 248 vs 759.6 +/- 220; p = 0.88). CD10 and CD13 MP's, as putative markers of RPTEC were also detected in response to TSP-1 exposure.


Our results show that MP's containing CD36 and CD47 are released from RPTEC upon exposure to TSP-1. CD36 MP's are significantly increased after TSP-1 exposure, whereas CD47 MP’s are statistically similar. It is known that CD-36 serves as a pro-inflammatory ligand for various inflammatory proteins including TSP-1; thus raising the possibility that TSP-1 exposure could initiate a cross-talk between renal epithelium and other targets/tissues mediated thru CD-36 ligand interactions. This is the first report that demonstrates the release of CD36 and CD47 postive MP’s in response to TSP-1 exposure. We propose that MP’s originating from kidney under pathological conditions could release pro-inflammatory signals to other remote organs.


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