Investigators at the Baylor College of Medicine reported in the November 17th issue of PNAS their ability to characterize a fibroblast precursor cell that may be involved in fibrotic ischemia/reperfusion cardiomyopathy (I/RC). The authors reported that the pathophysiology of I/RC, as a model of nonadaptive fibrosis, may be attributed to prolonged induction of the chemokine MCP-1 (monocyte chemoattractant protein). They noted that cardiac dysfunction could be prevented by overexpression of extracellular superoxide dismutase or by either gene deletion or injection of neutralizing antibodies to MCP-1. The data appear to implicate reactive oxygen and the continued expression of MCP-1 in generating I/RC. The data suggest that the cells involved in the pathology of I/RC are blood borne fibroblast precursors. These cells in serum-free cultures formed a spindled-shaped fibroblast morphology. Flow cytometric analysis found a subpopulation of precursor cells that were CD34+, CD45+, and expressed both collagen I and alpha smooth muscle actin. Adoptive transfer studies demonstrated a bone marrow origin for these precursors by establishing chimeric mice in which C57/Bl6 where irradiated and engrafted with ROSA 26 bone marrow-derived cells. The results also demonstrated that a serum factor, pentraxin SAP, which is closely related to C-reactive protein, inhibited fibrocyte differentiation in cultures. Similarly, SAP in vivo inhibited fibrosis in the I/RC model. Since both SAP and aggregated IgG binds to the FcγR, the experimental results suggest a regulatory role of FcγR in modulating in vitro the maturation of fibroblast precursor into fibrocytes. The authors concluded that SAP may provide a "potential link of non-adaptive fibrosis to inflammation and immunologic factors."