Postdoctoral Han: Sam68 regulation of macrophage function and arterial injury

Interventional treatment is widely used to treat patients with many diseases, such as cardiovascular disease. Along with the more and more popular application of the technique, the risks of the treatment are being paid more attention. Its risks are mainly caused by the vascular injury and mediated by re-endothelialization and neointima formation consisting inflammatory leukocytes. Recent studies have shown the potential value of strategies which targeted to decrease local inflammatory factors and accelerate re-endothelialization. Accumulated evidences indicate that inflammation cells contributed to the recovery of injured arteries, while NF-kB signal pathway is one of the most important pathway related to the inflammation, so the study on NF-kB activation to the recovery of the arterial injury is important. Recently study shows that Sam68 is required for NF-kB activation induction by TNFR. NF-kB activation is related to the re-endothelialization and neointima formation after carotid injury in mice, but it is still unknown whether sam68 plays a role in re-endothelialization and neointima formation or not. Recently preliminary studies from our lab show that Knockout of Sam68 accelerated the recovery of the arterial injury in mice and attenuate NF-kB activation in macrophage. Our further studies found a novel protein, Filamin A(FLNA), interacting with Sam68 upon TNFa stimulation in macrophage through Mass Spectrometry and CO-immunoprecipitation(CO-IP).