Skip to content
DraconiticResearch
Search Sources API
189,105 studies31 sourcesUpdated 7 min ago
Peer-reviewedCC BYFrontiers in immunology

Complement C1q promotes primary haemostasis in a microfluidic bleeding model

  • Peymane Zahiroddini1
  • Elaissa T. Hardy2
  • Yumiko Sakurai2
  • Wilbur A. Lam2
  • Marten Trendelenburg1
  1. 1Laboratory of Clinical Immunology, Department of Biomedicine, University of Basel , ,
  2. 2Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University , , ,
Read full textPDFDOICite

Abstract

Background: In systemic inflammatory diseases, thrombotic complications often cannot be fully explained by traditional risk factors, suggesting that the immune system directly affects hemostasis. The complement system, particularly C1q (the recognition molecule of the classical complement pathway), has been shown to enhance primary hemostasis in vivo and to bind von Willebrand factor (vWF) in vitro .

Aim: To investigate the role of the C1q-vWF interaction in human primary hemostasis.

Methods: We used a microfluidic bleeding model with endothelialized microchannels to visualize hemostatic processes in real-time. Following mechanical vessel injury, we tracked C1q deposition and its colocalization with vWF, platelets, and fibrinogen using confocal microscopy. The functional relevance of C1q was assessed using the C1q-inhibitory peptide 2J.

Results: C1q accumulates immediately at the injury site and exhibits strong colocalization with vWF and activated platelets, while colocalization with fibrinogen is minimal. Inhibiting C1q with peptide 2J significantly reduces both C1q and vWF deposition during early clot formation, and leads to prolonged bleeding time in this model.

Conclusion: Deposited C1q functions as a binding partner for vWF, enhancing primary hemostasis. This C1q-vWF axis may contribute to inflammation-related thromboembolic complications in humans.

Related

  1. Auxin‐Dependent Activation of RHD6‐RSL4 Cascade Promotes Root Hair Growth Under Boron Deficiency in Arabidopsis Primary Root Apices
    Cristina Bahamonde, Clara de la Osa, Jesús Rexach +6
    Plant Cell & EnvironmentPeer-reviewedCC BY5 citedPlant biologyOpenAlex
  2. Microfluidic models for adoptive cell-mediated cancer immunotherapies
    Giulia Adriani, Andrea Pavesi, Anthony T. Tan +3
    Drug Discovery TodayPeer-reviewedLicence not statedFull text66 citedImmunologyHAL
  3. High-throughput microfluidic encapsulation of cells in extracellular matrix microbeads for microtissue engineering.
    D. Mukherjee, M. Radecka-Rudzinska, K. Gizynski +3
    bioRxivPreprintAll rights reservedFull textSystems & synthetic biologybioRxiv
  4. A single microfluidic device for multi-omics analysis sample preparation
    Ranjith Kumar Ravi Kumar, Iman Haddad, Massamba Mbacké Ndiaye +3
    Lab on a ChipPeer-reviewedPublisher termsFull text1 citedBioinformatics & computational biologyHAL
  5. A microfluidic mother machine for high-throughput single-cell analysis of human leukemia T cells
    Simone Scalise, Giovanna Peruzzi, Davide Caprini +3
    Communications BiologyPeer-reviewedCC BY 4.0General biologyNatureCrossref

Cite

BibTeXRIS
BibTeX
@article{zahiroddini2026complement,
  title = {{Complement C1q promotes primary haemostasis in a microfluidic bleeding model}},
  author = {Peymane Zahiroddini and Elaissa T. Hardy and Yumiko Sakurai and Wilbur A. Lam and Marten Trendelenburg},
  journal = {Frontiers in immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1810209},
  url = {https://europepmc.org/article/PMC/PMC13671985},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Complement C1q promotes primary haemostasis in a microfluidic bleeding model
AU  - Peymane Zahiroddini
AU  - Elaissa T. Hardy
AU  - Yumiko Sakurai
AU  - Wilbur A. Lam
AU  - Marten Trendelenburg
PY  - 2026
DA  - 2026/10/02
JO  - Frontiers in immunology
DO  - 10.3389/fimmu.2026.1810209
UR  - https://europepmc.org/article/PMC/PMC13671985
AB  - Background: In systemic inflammatory diseases, thrombotic complications often cannot be fully explained by traditional risk factors, suggesting that the immune system directly affects hemostasis. The complement system, particularly C1q (the recognition molecule of the classical complement pathway), has been shown to enhance primary hemostasis in vivo and to bind von Willebrand factor (vWF) in vitro .  Aim: To investigate the role of the C1q-vWF interaction in human primary hemostasis.  Methods: We used a microfluidic bleeding model with endothelialized microchannels to visualize hemostatic processes in real-time. Following mechanical vessel injury, we tracked C1q deposition and its colocalization with vWF, platelets, and fibrinogen using confocal microscopy. The functional relevance of C1q was assessed using the C1q-inhibitory peptide 2J.  Results: C1q accumulates immediately at the injury site and exhibits strong colocalization with vWF and activated platelets, while colocalization with fibrinogen is minimal. Inhibiting C1q with peptide 2J significantly reduces both C1q and vWF deposition during early clot formation, and leads to prolonged bleeding time in this model.  Conclusion: Deposited C1q functions as a binding partner for vWF, enhancing primary hemostasis. This C1q-vWF axis may contribute to inflammation-related thromboembolic complications in humans.
SN  - 1664-3224
ER  -