Background: Monocyte accumulation contributes to inflammatory disease progression. Results: ASMCs overexpressing V3 resist monocyte adhesion by promoting elastogenesis, depleting hyaluronan, and reducing VCAM1, via differentially regulating TGF␤-, EGF-, and NFB-signaling pathways. Conclusion: V3 expression by ASMCs generates a microenvironment resistant to monocyte adhesion. Significance: Modifying ECM components via V3 expression alters monocyte adhesion, which suggests therapeutic possibilities to treat inflammation.

Background: Arterial smooth muscle cells (ASMCs) undergo phenotypic changes during pathophysiological processes. Results: V3 expression increases contractile SMC markers while decreasing a broad range of proinflammatory chemokines and transcription factors. Conclusion: V3 expression reprograms rat ASMCs promoting differentiated and anti-inflammatory phenotypes. Significance: Modifying ECM components via V3 expression could provide a potential therapeutic intervention against vascular and other diseases.