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High Phosphate-Induced JAK-STAT Signalling Sustains Vascular Smooth Muscle Cell Inflammation and Limits

Federica Macrì1, Ilaria Vigorito1, Stefania Castiglione1

  • 1Unit of Experimental Cardio-Oncology and Cardiovascular Aging, Centro Cardiologico Monzino-IRCCS, 20138 Milan, Italy.

Biomolecules
|January 23, 2024
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Summary

Vascular calcification involves inflammation. Blocking the JAK-STAT pathway reduced inflammation and increased calcium deposition in cells and mouse models, suggesting a new link.

Keywords:
JAK-STAThyperphosphataemiainflammationvascular calcificationvascular smooth muscle cells

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Area of Science:

  • Biomedical Science
  • Cardiovascular Research
  • Cell Biology

Background:

  • Vascular calcification (VC) is an age-related condition involving calcium-phosphate deposition in arteries.
  • Vascular smooth muscle cell (VSMC) osteogenic transformation drives VC.
  • The Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway is implicated in inflammation.

Purpose of the Study:

  • To investigate the role of the JAK-STAT signaling pathway in VSMC calcification.
  • To explore the relationship between inflammation and vascular calcification.

Main Methods:

  • Human aortic smooth muscle cells (HASMCs) were cultured in high phosphate (Pi) medium.
  • Calcium deposition was measured using Alizarin staining and colorimetric assays.
  • JAK-STAT pathway activation, inflammatory factor release, and gene expression were assessed. JAK-STAT inhibition was performed using JAK Inhibitor I in HASMCs and mouse aortic rings.

Main Results:

  • Pi-induced calcification in HASMCs led to the release of IL-6, IL-8, and MCP-1, and activation of JAK1-JAK3 and STAT1.
  • Phospho-STAT1 was observed in calcified murine aortas.
  • JAK-STAT pathway inhibition reduced HASMC proliferation and pro-inflammatory cytokine release but increased calcium deposition and RUNX2 expression, exacerbating aortic ring calcification.

Conclusions:

  • The JAK-STAT pathway plays a significant role in VSMC calcification.
  • Blocking the JAK-STAT cascade presents a potential therapeutic strategy for vascular calcification.
  • These findings suggest a novel connection between VSMC inflammation and vascular calcification.