Abstract
The development of intimal hyperplasia (IH) after coronary artery bypass graft (CABG) surgery significantly reduces the success rate of this procedure. Transforming growth factor-beta (TGFβ) promotes IH; however the underlying signalling mechanisms remain to be fully elucidated. We aimed to perform mechanistic characterisation of the ALK1 and ALK5 TGFβ signalling pathways in the context of vein graft failure. Wound healing and proliferation assays were performed in primary human saphenous vein SMCs (HSVSMC) treated with rTGFβ1 ± small molecule inhibitors of ALK1 (K02288) or ALK5 (SB525334). Although no effect on proliferation was observed, HSVSMC migration was significantly increased in the presence of SB525334, whereas K02288 treatment significantly reduced migration (p
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