Signaling pathway

Effects of ginsenoside Rg1 on the senescence of vascular smooth muscle cells

S. G. Li, Yan, M. Z., Zhang, D., Ye, M., Deng, J. J., Li, S. G., Yan, M. Z., Zhang, D., Ye, M., and Deng, J. J., “Effects of ginsenoside Rg1 on the senescence of vascular smooth muscle cells”, vol. 15, p. -, 2016.

The development of age-related cardiovascular disease is associated with the senescence of vascular cells. This study aimed to investigate the effect of ginsenoside Rg1 on vascular smooth muscle cell (VSMC) senescence. Primary VSMCs were cultured and divided into control, D-galactose (D-gal), Rg1-L, and Rg1-H groups, which were cultured without and with D-gal, and with low- and high-concentrations of Rg1, respectively. D-gal-induced cellular senescence was identified by b-galactosidase staining, and ultrastructural changes within the cells were observed.

Role of survivin in the pathogenesis of papillary thyroid carcinoma

J. Y. Li, Shi, J., Sang, J. F., Yao, Y. Z., Wang, X. C., and Su, L., “Role of survivin in the pathogenesis of papillary thyroid carcinoma”, vol. 14, pp. 15102-15111, 2015.

The purpose of this study was to assess the correlation between the survivin gene and the occurrence and pathogenesis of papillary thyroid carcinoma (PTC). Sixty patients with PTC and no preoperative chemotherapy were recruited for the study and 30 thyrophyma patients receiving operative treatment in Drum Tower Hospital (Nanjing, China) were included as the control group. The protein expression levels of survivin were assessed by immunoblotting and immunohistochemical analysis of tissues from both patient groups.

Smoking, aging, and expression of proteins related to the FOXO3 signaling pathway in lung tissues

Y. M. Yuan, Luo, L., Guo, Z., Yang, M., Lin, Y. F., and Luo, C., “Smoking, aging, and expression of proteins related to the FOXO3 signaling pathway in lung tissues”, vol. 14, pp. 8547-8554, 2015.

We investigated the effects of smoking and aging on pro­teins involved in the forkhead box O3 (FOXO3) signaling pathways in the lungs. Sixteen senescence-accelerated mouse-resistant 1 (SAMR1) and senescence-accelerated mouse-prone 8 (SAMP8) mice at 3 months of age were divided into a normally aged, smoke-exposed group (4 SAMR1 mice), a normally aged, air-exposed group (4 SAMR1 mice), an aging-accelerated, smoke-exposed group (4 SAMP8 mice), and an aging-accelerated, air-exposed group (4 SAMP8 mice).

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