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Plaque neovascularization

Our data demonstrate that silencing the expression of TPRC4 markedly reduced the cell proliferation, migration, and tube formation induced by oxLDL compared to the control group or NC group, indicating that silencing of TPRC4 could be a specific treatment to inhibit angiogenesis by reducing the number of proliferating cells. Studies have demonstrated that VEGF is required for adventitial angiogenesis and neovascularizationVEGF blocking suppresses physiological and pathological angiogenesis in various diseases In the present study, we found that silencing of TPRC4 significantly reduced the expression of VEGF; therefore, silencing of TPRC4 decreased the development of angiogenesis partly by reduction of VEGF. In addition, previous studies have suggested that suppression of TRPC4 inhibited activation of many signaling pathways that act downstream to VEGF to control angiogenesis, such as extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase (MAPK), and AKT signaling pathways The present study shows that TRPC4 inhibits the activation of NF-κB. NF-κB, an important transcription factor, is responsible for a variety of biological processes. Activation of constitutive NF-κB has been noted to mediate different biological functions, such as cell proliferation and angiogenesis [ Blockade of NF-κB signaling has been reported to inhibit angiogenesis by suppressing expression of VEGF in tumor cellsFurthermore, inhibition of NF-κB protects against atherosclerosis Our study verifies that suppression of TRPC4 prevents angiogenesis by inhibition of NF-κB in HCAECs, perhaps by modulating VEGF expression. However, further research is needed to confirm this