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Abstract: TH-PO329

Far Infrared Ray Irradiation Inhibits Platelet Aggregation Pathway Through Increasing ADAMTS13 Production to Cleave Length of von Willebrand Factor on Cell Surface and Decreasing Platelet Adhesion to Human Umbilical Vein Endothelial Cells

Session Information

  • Vascular Access - I
    November 07, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Dialysis

  • 704 Dialysis: Vascular Access


  • Hwang, Shang-Jyh, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
  • Chen, Wen-Yi, Kaohsiung Medical University Hospital, Kashsiung, Taiwan
  • Hwang, Daw-yang, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan

Far-infrared Ray (FIR),wavelength between 3-1000 μm, bears multiple effects on cardiovascular system and thrombogenesis. The von Willebrand factor (vWF), a large multimeric plasma glycoprotein as crucial player in arterial thrombus formation, can be cleaved by metalloprotease ADAMTS13 at its A2 domain cryptic in normal circulating vWF. We hypothesized FIR may induce ADAMTS13 release and decrease platelet adhesion to endothelial cells.


Cultured HUVECs treated with FIR irradiation for 30 minutes. Extracted mRNA and protein were measured by real time PCR, western blot, or ELISA. Supernatants were subjected to nonreducing gel electrophoresis to assess vWF multimer patterns by western blot. Platelet-HUVEC interactions were done by labeling platelet with calcein AM and co-cultured calcein AM-labeled platelet with FIR-treated or controlled HUVECs, followed by fluorescence microscopy analysis. Peripheral blood samples from 14 healthy volunteers before and after FIR irradiation were measured for ADAMTS13 by immunoassay and multimeric vWF pattern by SDS-agarose gel western blot.


The mRNA level of ADAMTS13 after FIR irradiation showed a time-duration dependent effect. FIR also stimulated ADAMTS13 but not vWF protein expressions in HUVECs. The levels of ADAMTS13 and vWF D4-CK domain in culture media measured showed increased after FIR irradiation. These findings reflected the possibility of vWF been cleaved from cell surface into medium, and it was demonstrated by the significantly reduced vWF D4-CK terminal expression on the surface of endothelial cells after FIR irradiation. The vWF multimer patterns in supernatants showed less presence of higher molecular weight forms, and binding of platelets to HUVEC cells was significantly reduced in FIR-treated cells. In healthy subjects, FIR irradiation increased blood levels of ADAMTS13 and reduced higher molecular weight forms of multimers of vWF.


We concluded FIR irradiation may inhibit platelet adhesion to endothelial cells via induction of ADAMTS13 which cleaves vWF on cell surface and results in decrease of platelet adhesion to endothelial cells. Our results provide information for further exploring the mechanisms of FIR in prevention of thrombus formation.


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