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Abstract: TH-PO377

5-HT1F Receptor Mediates Renal Vascular Homeostasis and Mitochondrial Biogenesis

Session Information

Category: Pharmacology (PharmacoKinetics, -Dynamics, -Genomics)

  • 1800 Pharmacology (PharmacoKinetics, -Dynamics, -Genomics)


  • Dupre, Tess, University of Arizona, Tucson, Arizona, United States
  • Schnellmann, Rick G., University of Arizona, Tucson, Arizona, United States

Acute kidney injury (AKI) is a disease with no treatment options. After AKI, there is a marked reduction in renal vasculature. Thus, promoting vascular recovery following AKI could facilitate renal repair as the vasculature is responsible for carrying oxygen and nutrients to extravascular tissues. Our laboratory has shown that stimulating mitochondrial biogenesis (MB) through the 5-HT1F receptor stimulates recovery from AKI. In contrast, 5HT1F receptor knockout mice have decreased MB, vascular content, and poor renal recovery. Importantly, induction of MB has been linked to increased angiogenesis. Thus, we hypothesized that the 5HT1F receptor mediates MB and plays a role in vascular homeostasis in renal endothelial cells.


Primary human glomerular endothelial cells (HEC) and mouse glomerular endothelial cells (MEC) were treated with the 5-HT1F receptor agonists 300nM LY344864 or 100 nM lasmiditan for 24 or 72h. Branching morphogenesis and wound healing were assessed via matrigel and scratch migration assays, respectively. Mitochondrial biogenesis was assessed by enumerating mitochondra via electron microscopy analysis.


Treatment of HEC and MEC with LY344864 or lasmiditan induced MB, as evidenced by increased mitochondrial number in comparison to vehicle treated cells. HEC that were treated with lasmiditan or LY344864 exhibited increased migratory capacity, as evidenced by increased endothelial branching (matrigel migration assays) and increased would healing (scratch closure).


Stimulation of 5-HT1F receptor with LY344864 and lasmiditan induces MB in HEC and MEC, and 5-HT1F receptor mediates angiogenic pathways. We propose that inducing MB in endothelial cells after AKI could restore vascular function and stimulate renal repair and recovery.


  • NIDDK Support