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. Author manuscript; available in PMC: 2013 Jun 18.
Published in final edited form as: Circulation. 2012 Feb 23;125(12):1533–1541. doi: 10.1161/CIRCULATIONAHA.111.078436

Figure 7.

Figure 7

Schematic illustration of the effects of targeted delivery of ECs over-expressing IL8RA and/or IL8RB on inflammatory mediator expression, neutrophil infiltration/activation and pro-inflammatory responses, and re-endothelialization and repair of blood vessels with endoluminal injury. (A) Native IL8RA and IL8RB on neutrophil membranes bind to IL8 with high affinity and play a critical role in neutrophil recruitment (e.g. adhesion and trans-endothelial migration) to sites of blood vessel injury. (B) ECs overexpressing IL8RA and/or IL8RB mimic the behavior of neutrophils that target and adhere to the sites of injury. (C) Proteolytic cleavage of collagen by matrix metalloproteinases (MMPs) generates an acetylated tripeptide, acPGP (Pro-Gly-Pro), which mimics key sequences of IL-8, stimulates IL8RA and IL8RB and prolongs influx of neutrophils.33,34 We postulate that IL8RA/RB-ECs compete with the binding of neutrophils to IL8 and/or the collagen fragment (Pro-Gly-Pro) expressed in injured tissue and thus inhibit neutrophil-induced inflammatory responses (e.g. infiltration of monocytes/macrophages and expression of pro-inflammatory cytokines) and accelerate healing of the injured tissue. IEL-internal elastic lamella; EEL-external elastic lamella; VSMC-vascular smooth muscle cell.