Injured blood vessels are repaired in part by bone marrow (BM)-derived progenitor cells, which migrate to the afflicted vessel and differentiate into new vascular cells. The chemokine SDF-1 attracts these cells and is reportedly produced by dying smooth muscle cells (SMCs). But the timing didn't add up. Production of SDF-1 by SMCs requires at least six hours, whereas the recruitment of progenitor cells begins within minutes of vessel injury.
Massberg et al. now account for the short time lag by showing that platelets–not previously thought to release SDF-1–provide an early burst of the chemokine that helps reel in the first progenitor cells. In fact, although SMCs eventually produced SDF-1, blocking platelet adherence completely prevented the recruitment of progenitor cells.
Platelet adherence was strictly required because the progenitor cells lacked the receptors necessary to tether them directly to the injured vessel wall. Instead, they glommed onto the aggregated platelets, an interaction that required the binding of P-selectin on the platelet to its ligand PSGL-1 on the progenitor cell.
The group is now investigating the recruited progenitor cell fate, which has never been convincingly established. Depending on what the cells become–either endothelial cells or SMCs–they could either help rebuild injured vessels or contribute to a dangerous vessel wall thickening.