Receptor for AGE (RAGE) mediates neointimal formation in response to arterial injury - PubMed (original) (raw)

. 2003 May 6;107(17):2238-43.

doi: 10.1161/01.CIR.0000063577.32819.23. Epub 2003 Apr 28.

Kai Wang, Marc S Penn, Steven P Marso, Michael A Lauer, Farhad Forudi, Xiaorong Zhou, Wu Qu, Yan Lu, David M Stern, Ann Marie Schmidt, A Michael Lincoff, Eric J Topol

Affiliations

• PMID: 12719284
• DOI: 10.1161/01.CIR.0000063577.32819.23

Receptor for AGE (RAGE) mediates neointimal formation in response to arterial injury

Zhongmin Zhou et al. Circulation. 2003.

Abstract

Background: Receptor for advanced-glycation end products (RAGE) and its ligands AGEs and S100/calgranulins have been implicated in a range of disorders. However, the role of RAGE/ligand interaction in neointimal hyperplasia after vascular injury remains unclear.

Methods and results: We examined the expression of RAGE and its ligands after balloon injury of the carotid artery in both Zucker diabetic and nondiabetic rats. Using a soluble portion of the extracellular domain of RAGE, we determined the effects of suppressing RAGE/ligand interaction on vascular smooth muscle cell (VSMC) proliferation and neointimal formation after arterial injury. We demonstrate a significantly increased accumulation of AGE and immunoreactivities of RAGE and S100/calgranulins in response to balloon injury in diabetic compared with nondiabetic rats. Blockade of RAGE/ligand interaction significantly decreased S100-stimulated VSMC proliferation in vitro and bromodeoxyuridine (BrdU)-labeled proliferating VSMC in vivo, and suppressed neointimal formation and increased luminal area in both Zucker diabetic and nondiabetic rats.

Conclusions: These findings indicate that RAGE/ligand interaction plays a key role in neointimal formation after vascular injury irrespective of diabetes status and suggest a novel target to minimize neointimal hyperplasia.

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