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Yi-Hsin Lien,Jhaol-Huei Wu,Jiunn-Wang Liao,Tzong-Ming Wu 한국고분자학회 2013 Macromolecular Research Vol.21 No.5
Thermosensitive and magnetic nanoparticles as “smart” drug carriers have shown great potential in the field of controlled drug delivery owing to their unique properties. Previously, poly(N-isopropylacrylamide)-coated silica/magnetic nanoparticles (PNIPAM/SiO2/Fe3O4 nanoparticles) were synthesized using SiO2-coated Fe3O4 nanoparticles as a template. The properties of these nanoparticles such as the transition of the lower critical solution temperature (LCST), biocompatibility, drug loading efficiency, and drug release kinetics were investigated in vitro for both targeted and controlled drug delivery. The release profile and the in vitro cancer cell inhibition activity of vitamin D3 loading for PNIPAM/SiO2/Fe3O4 nanoparticles were systemically studied. The loading and release behavior of vitamin D3 were found to be dependent on the LCST of PNIPAM/SiO2/Fe3O4 nanoparticles. HepG2 liver cancer cells were incubated with PNIPAM/SiO2/Fe3O4 nanoparticles loaded with vitamin D3 for 5 days, and cell viability significantly decreased, as observed by 3-(4,5-cimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assays, which was further confirmed by transmission electron microscopy (TEM)images. In conclusion, the current study demonstrated that PNIPAM/SiO2/Fe3O4 nanoparticles can be used as potential drug delivery systems for controlled release.
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Wu Szu-Hsien,Yu Jin-Huei,Liao Yu-Ting,Liu Kuo-Hao,Chiang En-Rung,Chang Ming-Chau,Wang Jung-pan 한국조직공학과 재생의학회 2022 조직공학과 재생의학 Vol.19 No.3
BACKGROUND: Infant adipose-derived mesenchymal stem cells (ADSCs) collected from excised polydactyly fat tissue, which was surgical waste, could be cultured and expanded in vitro in this study. In addition, the collecting process would not cause pain in the host. In this study, the proliferation, reduction of senescence, anti-oxidative ability, and differentiation potential in the infant ADSCs were compared with those in the adult ADSCs harvested from thigh liposuction to determine the availability of infant ADSCs. METHODS: Proliferation was determined by detecting the fold changes in cell numbers and doubling time periods. Senescence was analyzed by investigating the age-related gene expression levels and the replicative stress. The superoxide dismutase (SOD) gene expression, adipogenic, neurogenic, osteogenic, and tenogenic differentiation were compared by RTqPCR. The chondrogenic differentiation efficiency was also determined using RT-qPCR and immunohistochemical staining. RESULTS: The proliferation, SOD (SOD1, SOD2 and SOD3) gene expression, the stemness-related gene (c-MYC) and telomerase reverse transcriptase of the infant ADSCs at early passages were enhanced compared with those of the adults’. Cellular senescence related genes, including p16, p21 and p53, and replicative stress were reduced in the infant ADSCs. The adipogenic genes (PPARc and LPL) and neurogenic genes (MAP2 and NEFH) of the infant ADSC differentiated cells were significantly higher than those of the adults’ while the expression of the osteogenic genes (OCN and RUNX) and tenogenic genes (TNC and COL3A1) of both demonstrated opposite results. The chondrogenic markers (SOX9, COL2 and COL10) were enhanced in the infant ADSC differentiated chondrogenic pellets, and the expression levels of SODs were decreased during the differentiation process. CONCLUSION: Cultured infant ADSCs demonstrate less cellular senescence and replicative stress, higher proliferation rates, better antioxidant defense activity, and higher potential of chondrogenic, adipogenic and neurogenic differentiation.
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Hung-Jen Liu,Ping-Yuan Lin,Ling-Rung Wang,Hsue-Yin Hsu,Ming-Huei Liao,Wen-Ling Shih 한국분자세포생물학회 2008 Molecules and cells Vol.26 No.4
The first ORF of the ARV S1133 S1 segment encodes the nonstructural protein p10, which is responsible for the induction of cell syncytium formation. However, p10-dependent signaling during syncytium formation is fully unknown. Here, we show that dominant negative RhoA, Rho inhibitor C3 exoenzyme, ROCK/Rho-kinase inhibitor Y-27632 and Rac1 inhibitor NSC23766 inhibit p10-mediated cell fusion. p10 over-expression is concomitant with activation and membrane translocation of RhoA and Rac1, but not cdc42. RhoA and Rac1 downstream events, including JNK phosphorylation and transcription factor AP-1 and NF-B activation, as well as MLC expression and phosphorylation are simultaneously activated by p10. p10 point mutant T13M possessed 20% fusion-inducing ability and four p10 fusion-deficient mutants V15M, V19M, C21S and L32A reduced or lost their ability to activate RhoA and Rac1 signaling. We conclude that p10-mediated syncytium formation proceeds by utilizing RhoA and Rac1-dependent signaling.
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