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Related Experiment Video

Updated: May 12, 2026

Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion

Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion

Published on: June 15, 2019

Targeting complement component 5a promotes vascular integrity and limits airway remodeling.

Mohammad A Khan¹, Christian Maasch, Axel Vater

¹Medical Service, Veterans Affairs Palo Alto Health Care System, Palo Alto, CA 94304, USA.

Proceedings of the National Academy of Sciences of the United States of America

|March 27, 2013

Summary

Blocking complement component 5a (C5a) improved microvascular injury in C3-deficient transplant recipients. Targeting C5a may benefit transplant health, especially when C3 inhibitors are used.

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Last Updated: May 12, 2026

Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion

Evaluation of the Interplay Between the Complement Protein C1q and Hyaluronic Acid in Promoting Cell Adhesion

Published on: June 15, 2019

A Rat Carotid Balloon Injury Model to Test Anti-vascular Remodeling Therapeutics

A Rat Carotid Balloon Injury Model to Test Anti-vascular Remodeling Therapeutics

Published on: September 19, 2016

Area of Science:

Immunology
Transplantation Biology
Vascular Biology

Background:

Allograft rejection increases microvascular dilatation and permeability, compromising transplant health.
Complement component 3 (C3) inhibition is typically vasculoprotective, but C3 deficiency can paradoxically worsen microvascular injury during rejection.
In C3 deficiency, thrombin activity generates C5a, promoting vasodilatation and permeability.

Purpose of the Study:

To investigate the role of thrombin and C5a in microvascular injury during C3-deficient allograft rejection.
To evaluate the therapeutic potential of C5a inhibition in preventing transplant-associated microvascular damage.

Main Methods:

Assessed microvessel thrombin deposition and plasma C5a levels in C3(-/-) transplant recipients during acute rejection.
Administered a C5a inhibitor (NOX-D19) to C3(-/-) airway transplant recipients.
Evaluated tissue oxygenation, vascular leakiness, and airway ischemia.

Main Results:

C3(-/-) recipients showed increased microvessel thrombin deposition, elevated C5a, vasodilatation, and vascular permeability.
NOX-D19 treatment significantly improved tissue oxygenation and reduced microvascular leakiness.
C5a inhibition prevented airway ischemia in C3(-/-) recipients, independent of T-cell immunosuppression.

Conclusions:

Thrombin-mediated C5a generation contributes to microvascular injury in C3-deficient allograft rejection.
Targeting C5a offers a promising therapeutic strategy to protect vascular integrity in transplantation.
Combined inhibition of C3 and C5a pathways may enhance clinical outcomes in transplant recipients.