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effects of TRPC4 on oxLDL-induced in vitro angiogenesis

TRPC proteins, as non-selective cation channels, are ubiquitously expressed throughout the cardiovascular systemThey significantly contribute to various human physiological and pathophysiological cardiovascular diseases by the functioning of Ca2+/Na+ permeable channels and/or signaling platforms Endothelial cytosolic Ca2+ plays a significant role in the process of angiogenesis. Nilius et al. have confirmed the potential roles of TRP-mediated Ca2+ influx in the angiogenic process . These pathologies are directly or indirectly related to the development of atherosclerotic lesions. With the development of atherosclerotic lesion, new vessels sprouting from the adventitia neovascularize the growing plaque. Inflammatory cells could be recruited through neovascularization, leading to exacerbation of inflammatory state and acceleration of plaque growth even in-stent restenosis (ISR) Plaque neovascularization is thought to contribute to the plaque instability, and ultimately results in thromboembolic complications Therefore, the functional roles of TRPCs in neovascularization have received great attention in recent years Previous studies have suggested that TRPC6 plays key roles in growth-factor-induced angiogenesis during plaque neovascularization In addition to TRPC6, TRPC4 has recently been attracting increased research attention. TRPC4, an essential component of the nonselective calcium-permeable cation channel, is assumed to be activated by Gq/phospholipase C-coupled receptors and tyrosine kinases [ and it is associated with multiple processes, including cell proliferation, endothelial permeability, vasodilation, and neurotransmitter release Song et al. confirmed that suppression of TPRC4 inhibits retinal neovascularization [. Given the multiple functions of TPRC4, we hypothesized that TPRC4 might play a critical role in angiogenesis involved in atherosclerosis.

In the present study, the silencing effects of TRPC4 on oxLDL-induced in vitro angiogenesis were investigated, as well as the underlying molecular mechanisms involved in these effects. Our data showed that silencing of TRPC4 significantly attenuated angiogenesis induced by oxLDL in HCAECs by reducing cell proliferation, migration, and tube formation. The underlying mechanisms might be associated with modulation of the expression levels of VEGF and NF-κB p65. These results suggest that suppression of TRPC4 might be an alternative therapeutic strategy for atherosclerotic neovascularization.