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Abstract: SA-PO031

An Open Microfluidic Model to Investigate Podocyte-Parietal Epithelial Cell Cross-Talk In Vitro

Session Information

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

Category: Bioengineering

  • 300 Bioengineering


  • Zeng, Yuting, University of Washington Department of Chemistry, Seattle, Washington, United States
  • Pippin, Jeffrey W., University of Washington Division of Nephrology, Seattle, Washington, United States
  • Shankland, Stuart J., University of Washington Division of Nephrology, Seattle, Washington, United States
  • Theberge, Ashleigh B., University of Washington Department of Chemistry, Seattle, Washington, United States

Although focal segmental glomerulosclerosis (FSGS) is initially caused by direct injury to podocytes, their neighboring parietal epithelial cells (PECs) also undergo secondary molecular changes that further damage the glomerulus. The crosstalk between injured podocytes and PECs is poorly understood, in part due to a lack of appropriate experimental models for study. The goal of this study is to establish an in vitro coculture model to determine what mediators derived from injured podocytes cause PECs damage.


We engineered a novel open microfluidic coculture device where two culture chambers are separated by a half wall that can be connected to study intercellular interactions. Diffusion calculations suggested that moderate sized (10 kDa) signaling molecules take ~ 2 d to reach the other chamber via diffusion. In mouse podocyte-PEC coculture studies, immortalized mouse podocytes were exposed to cytotoxic sheep anti-podocyte antibodies, puramycin, or Adriamycin, and cocultured with mouse PECs for up to 96 h. In human podocyte studies, primary human podocytes were also injured with anti-podocyte antibodies, puramycin, or Adriamycin. Podocyte responses were assessed by phase-contrast imaging, MTT assays, and immunostaining. Immunostaining also measured PEC activation and epithelial-mesenchymal transition (EMT).


Immediatly following podocyte injury, both mouse and human podocytes displayed foot process effacement and cell body shrinkage. In addition, cell viability was decreased of injured podocytes. The normal contiguous monolayer of mouse podocytes was disrupted, accompanied by a dose-dependent increase in the de novo expression of the injury marker desmin, and a decrease in the cytockeletal marker F-actin along the cell borders. In podocyte-PEC coculture, PECs were activated (expressed CD44) accompanied by increased SM22, an EMT marker. A time course of bulk RNA seq results are pending.


This novel in vitro microfluidic model for coculturing injured podocytes and neighboring cells has the potential to study many pathways involved in podocyte-related intercellular crosstalk, glomerular disease mechanisms, and drug screening.


  • NIDDK Support