Early fibroblast progenitor cell migration to the AngII-exposed myocardium is not CXCL12 or CCL2 dependent as previously thought.

Fibroblast progenitor cells (fibrocytes) are important to the development of myocardial fibrosis and are suggested to migrate to the heart via CXCL12 and chemokine ligand (CCL) 2. We hypothesized that if these chemokines are recruiting fibrocytes, disrupting their signaling will reduce early (3-day) fibrocyte infiltration and, consequently, fibrosis in the myocardium. C57/Bl6 and CCR2(-/-) mice were infused with saline or angiotensin (Ang) II, with or without CXC receptor 4 blockade (AMD3100).

Neutrophils are responsible for impaired medial smooth muscle cell recovery and exaggerated allograft vasculopathy in aortic allografts exposed to prolonged cold ischemia.

Background: Ischemia and reperfusion injury is critical in allograft vasculopathy (AV) development. We have shown that neutrophil-mediated medial smooth muscle cell (SMC) loss precedes AV and that prolonged cold ischemia (CI) impairs medial SMC recovery and accelerates AV development. We hypothesize that neutrophils (NØs) are responsible for failed medial SMC recovery that precedes AV.

Contribution of B cells and antibody to cardiac allograft vasculopathy.

Background: The aim of this study was to determine the role of alloantibody in the development of cardiac allograft vasculopathy (AV). AV is the main pathologic indicator of chronic cardiac graft rejection resulting in graft loss at 10 years posttransplant. In AV, a neointimal lesion forms resulting in luminal occlusion and damage to the transplanted organ.