Roles of Bone-Marrow-Derived Cells and Inflammatory Cytokines in Neointimal Hyperplasia after Vascular Injury

Abstract

Bone-marrow-derived cells can generate vascular progenitor cells that contribute to pathological remodeling in models of restenosis after percutaneous coronary intervention (PCI). We created models of vascular injury in mice with bone marrow transplants (BMT) to determine relationships between bone-marrow-derived cells and subsequent biological factors. Mesenchymal stromal cells (MSCs) seemed to inhibit the inflammatory reaction and help stabilize injured vascular regions through mobilizing more endogenous bone-marrow-derived (EBMD) cells to the peripheral circulation. Granulocyte-colony stimulating factor (G-CSF) mobilized more EBMD cells to the peripheral circulation, and they accumulated on the injured side of the vascular lumen. The inflammatory cytokines, tumor necrosis factor (TNF)-alpha, and interleukin (IL)-6 mobilized EBMD cells that play an important role in the process of neointimal hyperplasia after vascular injury. These factors might comprise a mechanism that alters the transdifferentiation or paracrine capabilities of EBMD cells and are potential targets of treatment for patients with cardiovascular diseases.