Background and purpose: Recent studies have shown that resveratrol increased endothelial progenitor cells (EPCs) numbers and functional activity. However, the mechanisms remain to be determined. Previous studies have demonstrated that increased EPC numbers and activity were associated with the inhibition of EPC senescence, which involves activation of telomerase. Therefore, we investigated whether resveratrol inhibits the onset of EPC senescence through telomerase activation, leading to potentiation of cellular activity. Experimental approach: After prolonged in vitro cultivation, EPCs were incubated with or without resveratrol. The senescence of EPCs were determined by acidic b-galactosidase staining. The bromo-deoxyuridine incorporation assay or a modified Boyden chamber assay were employed to assess proliferative or migratory capacity, respectively. To further examine the underlying mechanisms of these effects, we measured telomerase activity and the phosphorylation of Akt by western blotting. Key results: Resveratrol dose dependently prevented the onset of EPCs senescence and increased the proliferation and migration of EPCs. The effect of resveratrol on senescence could not be abolished by eNOS inhibitor or by an oestrogenic receptor antagonist. Resveratrol significantly increased telomerase activity and Akt phosphorylation. Pre-treatment with the PI3K inhibitor, LY294002, significantly attenuated resveratrol-induced telomerase activity. Conclusions and implications:Resveratrol delayed the onset of EPC senescence and this effect was accompanied by activation of telomerase through the PI3K-Akt signalling pathway. The inhibition of EPCs senescence by resveratrol might protect EPCs against dysfunction induced by pathological factors in vivo and improve EPC functional activities in a way that may be important for cell therapy.

Colorectal cancer (CRC) is one of the leading causes of cancer death worldwide, and metastasis is the major cause of CRC-related mortality. Transforming growth factor-beta (TGF-β) has a central role not only in the regulation of the normal colon but also in the development and metastasis of CRC. However, TGF-β is not considered an ideal therapeutic target because it shows both pro-tumorigenic and anti-tumorigenic activity, depending on the tumor stage. Therefore, it is important to find a downstream signaling component of TGF-β that can be targeted to impair CRC metastasis. Here, we show that TGF-β promotes CRC migration and upregulates the expression of long-noncoding RNA Taurine Upregulated Gene 1 (TUG1). TUG1 knockdown inhibited migration, invasion, and epithelial–mesenchymal transition (EMT) of CRC cells in vitro, and reduced CRC lung metastasis in vivo. TGF-β induced metastasis, and TUG1 knockdown inhibited these effects. In addition, TGF-β could not reverse the anti-metastasis effects of TUG1 knockdown. These data demonstrate that TUG1 is a downstream molecular of TGF-β. Moreover, TWIST1 expression was increased with TGF-β treatment, and TUG1 knockdown decreased TWIST1 expression in CRC cells. TWIST1 knockdown inhibited invasion and EMT in CRC cells; these effects were not changed by simultaneous TUG1 knockdown, indicating that TWIST1 is a downstream mediator of TUG1. Moreover, TUG1 was significantly overexpressed in CRC patients. In conclusion, TGF-β promotes metastasis of CRC via a TUG1/TWIST1/EMT signaling pathway. TUG1 may be a promising drug target to inhibit TGF-β pathway activation in the treatment of CRC.

Stem cell transplantation has become a promising therapeutic approach for the treatment of myocardial infarction (MI). However, the poor survival of the donor cells after transplantation has restricted its therapeutic efficacy. Hydrogen sulfide (H 2 S), one gaseous signaling molecule, has been applied to inhibit cell apoptosis and promote cell survival. In the present study, we therefore examined the effects of H 2 S on the survival of mesenchymal stem cells (MSCs). MSCs were isolated from the femur of male Sprague-Dawley rats (about 4 weeks old, 100 g). Preconditioning MSCs with 200 μmol/L NaHS (as the donor of H 2 S) for 30 min decreased the hypoxia-induced cell apoptosis in vitro. The mechanisms contributing to the beneficial effects of H 2 S on MSCs were associated with increased levels of phosphorylated Akt (pAkt), phosphorylated Erk1/2 (pErk1/2) and phosphorylated glycogen synthase kinase-3β (pGSK-3β) in MSCs. Subsequently, MSCs (1 × 10 6 ), MSCs preconditioned with H 2 S (1 × 10 6 ), or phosphate buffered saline (PBS) were injected into rat hearts immediately after MI (the ligation of the left anterior descending of coronary artery). Real-time PCR for the Sry gene, located on the Y chromosome, indicated that preconditioning with H 2 S improved the survival rate of the transplanted MSCs in infarcted myocardium 4 days after MI, compared with the untreated MSCs. Furthermore, transplantation of the H 2 S-pretreated MSCs reduced the infarct size and increased left ventricular (LV) function, as judged by transthoracic echocardiography. In conclusion, H 2 S preconditioning effectively promotes MSCs survival under ischemic injury and helps cardiac repair after MI, which has great clinical significance.

Collagen and collagen peptides are widely used as cosmetic ingredients. In the present study, acid-solubilized collagen (ASC) and pepsin-solubilized collagen (PSC) were extracted from giant croaker (Nibea japonica) skin. The proline hydroxylation rates of ASC and PSC were 38.1% and 39.3%. The denaturation temperatures (Td) were approximately 34.5 °C for both ASC and PSC. The results of sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and fourier transform infrared spetroscopy (FTIR) demonstrated that ASC and PSC were mainly type I collagen. Furthermore, As, Pb and Hg contents in the extracted collagen were lower than the national standards of China. In addition, collagen had good moisture absorption and retention properties when compared to glycerol. The collagen was also not cytotoxic to NIH-3T3 fibroblast cells, indicating that Nibea japonica skin collagen can be utilized in cosmetic applications.