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1.
Chinese Journal of Tissue Engineering Research ; (53): 1177-1183, 2015.
Article in Chinese | WPRIM | ID: wpr-460683

ABSTRACT

BACKGROUND:Rat tail colagen type I can promote the increase of muscle fiber cels and migration and tube formation of endothelial cels, which is speculated to provide a more suitable internal environment for the growth of cels. OBJECTIVE:To observe the effect and safety of platelet-derived growth factor-BB (PDGF-BB) with rat rail colagen against apoptosis of human umbilical vein endothelial celsin vitro. METHODS:The passage 4 human umbilical vein endothelial cels were cultured in the medium of rat rail colagen and the reduction ratio in different time points was detected by Alamar Blue. The passage 4 human umbilical vein endothelial cels were divided into four groups and cultured in 24-wel culture plates: control group, PDGF-BB group, H2O2 group, PDGF-BB+colagen group. H2O2 was used to induce cel apoptosis in al the groups. Western blot was used to detect the expression of PDGF-BB, apoptosis-related protein and anti-apoptosis protein after 72 hours. Meanwhile, TUNEL method was used to detect cel apoptotic rate. RESULTS AND CONCLUSION:The tube formation in the human umbilical vein endothelial cels was more than that cultured in normal medium (P < 0.05). Cels cultured with rat tail colagen showed similar growth to normal control cels, indicating rat tail colagen had no cytotoxicity. The expressions of PDGF-BB, Bcl-2, and p-Akt in the PDGF-BB+colagen group were significantly higher than those in the other three groups (P < 0.05), but the expression of Bax was lower than that in the other three groups (P < 0.05). The apoptotic rate in the PDGF-BB+colagen group was lower than the PDGF-BB group and H2O2 group (P < 0.05). These findings indicate that rat tail colagen has no cytotoxicity to human umbilical vein endothelial cells, and rat tail collagen combined with PDGF-BB can predominantly enhance anti-apoptosis effects.

2.
Chinese Journal of Tissue Engineering Research ; (53): 199-204, 2014.
Article in Chinese | WPRIM | ID: wpr-443640

ABSTRACT

BACKGROUND:Cyclin A2 is a key regulator of cellcycle. Location and expression of cyclin A2 in neonatal mouse myocardium is not clear. OBJECTIVE:To observe the location and expression of cyclin A2 in neonatal mouse cardiomyocytes and its relationship with the exit of cardiomyocytes from cellcycle. METHODS:Neonatal mice were kil ed to take myocardial tissues at 0, 3, 7, 14 and 28 days after birth. Western blot were used to detect the expression of cyclin A2, proliferating cellnucleus antigen and Phospho-histone H3. Immunohistochemitry detection was used to detect the location of cyclin A2 and expression of proliferation cellnucleus antigen at different time after birth. RESULTS AND CONCLUSION:Western blot showed the decrease of cyclin A2 after birth til disappeared at day 4 (P=0.001). Cyclin A2 located mainly in the nucleus after birth and exported to the cytoplasm at day 14, and basical y disappeared at day 28. Proliferating cellnucleus antigen showed gradual y decreased tendency after birth. Mitosis specific marker, Phospho-histone H3, exhibited a gradual decrease after birth, which was consistent with cyclin A2 in expression intensity.

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