Toll-like receptor 2-deficiency on bone marrow-derived cells augments vascular healing of murine arterial lesions

Publication date: Available online 28 December 2019Source: Life SciencesAuthor(s): W. Liu, J.-C. Eczko, M. Otto, R. Bajorat, B. Vollmar, J.-P. Roesner, N.-M. WagnerAbstractAimsNeointimal hyperplasia contributes to arterial restenosis after percutaneous transluminal coronary angioplasty or vascular surgery. Neointimal thickening after arterial injury is determined by inflammatory processes. We investigated the role of the innate immune receptor toll-like receptor 2 (TLR2) in neointima formation after arterial injury in mice.Materials and methodsCarotid artery injury was induced by 10% ferric chloride in C57Bl/6J wild type (WT), TLR2 deficient (B6.129-Tlr2tm1Kir/J, TLR2−/−) and WT mice treated with a TLR2 blocking antibody. 21 days after injury, carotid arteries were assessed histomorphometrically and for smooth muscle cell (SMC) content. To identify the contribution of circulating cells in mediating the effects of TLR2-deficiency, arterial injury was induced in WT/TLR2−/−-chimeric mice and the paracrine modulation of bone marrow-derived cells from WT and TLR2−/− on SMC migration compared in vitro.Key findingsTLR2−/− mice and WT mice treated with TLR2 blocking antibodies exhibited reduced neointimal thickening (23.7 ± 4.2 and 6.5 ± 3.0 vs. 43.1 ± 5.9 μm, P < 0.05 and P < 0.01), neointimal area (5491 ± 1152 and 315 ± 76.7 vs. 13,756 ± 2627 μm2, P < 0.05 and P < 0.01) and less luminal stenosis c...
Source: Life Sciences - Category: Biology Source Type: research