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Guo Li,
Xiao-Ai Zhang,
Hua Wang,
Xin Wang,
Chun-Ling Meng, Chu-Yan Chan,
David Tai Wai Yew,
Kam Sze Tsang,
Karen Li,
Sau-na Tsai,
Sai-Ming Ngai,
Zhong Chao Han,
Marie Chia-Mi Lin,
Ming-Liang He,
Hsiang-Fu Kung
[show abstract]
[hide abstract]
ABSTRACT: Umbilical cord (UC) and placenta (P) have been suggested as alternatives to bone marrow (BM) as sources of mesenchymal stem
cells (MSC) for cell therapy, with both UC- and P-MSC possess immunophenotypic and functional characteristics similar to BM-MSC.
However, under defined conditions, the migration capacity of BM- and P-MSC was found to be 5.9- and 3.2-folds higher than
that of UC-MSC, respectively. By the use of 2-DE and combined MS and MS/MS analysis, six differentially expressed proteins
were identified among these MSC samples, with five of them known to be involved in cell migration as migration enhancing or
inhibiting proteins. Interestingly, the expression levels of those proteins reflect perfectly the migration capacity of corresponding
MSC, which is also proved by in vitro overexpression and silencing techniques. Our study indicates that a bunch of migration-related
proteins are pivotal in governing the migration capacity of MSC.
12/2011: pages 51-68;
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Guo Li,
Xiao-Ai Zhang,
Hua Wang,
Xin Wang,
Chun-Ling Meng, Chu-Yan Chan,
David Tai Wai Yew,
Kam Sze Tsang,
Karen Li,
Sau-Na Tsai,
Sai-Ming Ngai,
Zhong Chao Han,
Marie Chia-Mi Lin,
Ming-Liang He,
Hsiang-Fu Kung
[show abstract]
[hide abstract]
ABSTRACT: Umbilical cord (UC) and placenta (P) have been suggested as alternatives to bone marrow (BM) as sources of mesenchymal stem cells (MSC) for cell therapy, with both UC- and P-MSC possess immunophenotypic and functional characteristics similar to BM-MSC. However, under defined conditions, the migration capacity of BM- and P-MSC was found to be 5.9- and 3.2-folds higher than that of UC-MSC, respectively. By the use of 2-DE and combined MS and MS/MS analysis, six differentially expressed proteins were identified among these MSC samples, with five of them known to be involved in cell migration as migration enhancing or inhibiting proteins. Interestingly, the expression levels of those proteins reflect perfectly the migration capacity of corresponding MSC, which is also proved by in vitro overexpression and silencing techniques. Our study indicates that a bunch of migration-related proteins are pivotal in governing the migration capacity of MSC.
Advances in experimental medicine and biology 01/2011; 720:51-68. · 1.09 Impact Factor
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[show abstract]
[hide abstract]
ABSTRACT: Umbilical cord (UC) and placenta (P) are generally believed to be potential alternatives to bone marrow (BM), as sources of mesenchymal stem cells (MSC) for cell therapy. They possess immunophenotypic and functional characteristics which are similar to that of BM-MSC, yet one of the crucial factors in determining the tissue regeneration process--the migration capacity--is still unclear. In our previous study, the migration capacity of BM- and P-MSC was found 5.9- and 3.2-fold higher than that of UC-MSC, respectively. By using 2-dimensional gel electrophoresis (2-DE) and combined MS and MS/MS analysis, six proteins were identified as differentially expressed among these MSC samples. Five out of the six proteins were known to be involved in cell migration as migration inhibiting or enhancing proteins.
Methods in molecular biology (Clifton, N.J.) 01/2011; 698:443-57.
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[show abstract]
[hide abstract]
ABSTRACT: Umbilical cord (UC) and placenta (P) are generally believed to be potential alternatives to bone marrow (BM), as sources of
mesenchymal stem cells (MSC) for cell therapy. They possess immunophenotypic and functional characteristics which are similar
to that of BM-MSC, yet one of the crucial factors in determining the tissue regeneration process – the migration capacity
– is still unclear. In our previous study, the migration capacity of BM- and P-MSC was found 5.9- and 3.2-fold higher than
that of UC-MSC, respectively. By using 2-dimensional gel electrophoresis (2-DE) and combined MS and MS/MS analysis, six proteins
were identified as differentially expressed among these MSC samples. Five out of the six proteins were known to be involved
in cell migration as migration inhibiting or enhancing proteins.
Key wordsMesenchymal stem cells-Migration-2-Dimensional gel electrophoresis-MS and MS/MS analysis
12/2010: pages 443-457;
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Yangchao Chen,
Dan Xie,
Wing Yin Li,
Chi Man Cheung,
Hong Yao,
Ching Yu Chan, Chu-yan Chan,
Fang-Ping Xu,
Yan-Hui Liu,
Joseph J Y Sung,
Hsiang-fu Kung
[show abstract]
[hide abstract]
ABSTRACT: The function of EZH2 in tumorigenesis and liver metastasis of pancreatic cancer has never been elucidated in vivo. EZH2 was overexpressed in pancreatic carcinomas and its overexpression was associated with tumor differentiation and pT status. Suppression of EZH2 caused a significant growth inhibition of pancreatic cancer cells in vitro and markedly diminished their tumorigenicity in vivo. Knock-down of EZH2 inhibited liver metastasis of pancreatic cancer in vivo. EZH2 has a crucial role in tumor growth and liver metastasis of pancreatic cancer.
Cancer letters 11/2010; 297(1):109-16. · 4.86 Impact Factor
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[show abstract]
[hide abstract]
ABSTRACT: zMicroRNAs (miRNAs) are endogenously expressed small noncoding RNAs that regulate approximately one-third of human genes at post-transcription level. Previous studies have shown that miRNAs were implicated in many cellular processes and participated in the progress of various tumors including hepatocellular carcinoma (HCC). Among all miRNAs, the let-7 family is well recognized to play pivotal roles in tumorigenesis by functioning as potential growth suppressor. In the present study, we aimed to investigate the role of let-7 family, particularly the hsa-let-7g, in the molecular pathogenesis of HCC. By use of MTT, qPCR, Western blotting and 2-dimensional electrophoresis (2-DE), over-expression of hsa-let-7g was found to inhibit the proliferation of HCC cell line via negative and positive regulations of c-Myc and p16(INK4A) , respectively. The expression of hsa-let-7g was noted to be markedly lowered in the HepG2, Hep3B and Huh7 cells, yet higher in the Bel-7404 HCC cell line. Proliferation of HCC cell line was significantly inhibited after the transfection of hsa-let-7g mimics, while hsa-let-7g inhibitor transfection exerted an opposite effect. Concurrently, the mRNA and protein levels of c-Myc were found significantly decreased in HepG2 cells after transfection of hsa-let-7g mimics, but obviously increased in Bel-7404 cells after transfection of hsa-let-7g inhibitor. As revealed by 2-DE, a significant upregulation of p16(INK4A) was revealed after the gain-of-function study using hsa-let-7g. Therefore, we suggest that hsa-let-7g may act as a tumor suppressor gene that inhibits HCC cell proliferation by downregulating the oncogene, c-Myc, and upregulating the tumor suppressor gene, p16(INK4A) .
International Journal of Cancer 03/2010; 128(2):319-31. · 5.44 Impact Factor
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[show abstract]
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ABSTRACT: Fructus Ligustri Lucidi (FLL) has been used in traditional Chinese medicine for over 1000 years. The ethanol extract of FLL (EFLL) has been shown to be a potential candidate in the prevention and treatment of osteoporosis. The present study aimed to determine whether EFLL carries out the effect by promoting osteogenesis in mesenchymal stem cells (MSCs). The osteogenic differentiation of MSCs was evaluated by their alkaline phosphatase (ALP) activities and mineralization. Expression of genes was detected by RT-PCR. We found that EFLL significantly stimulated the ALP activities and shortened the time needed for the mineralization of MSCs during osteogenic differentiation. The expression of several osteoblast differentiation regulators was also upregulated by EFLL during this process. Our study demonstrated that the EFLL is capable of enhancing osteogenic differentiation of MSCs. It might be useful for treating diseases with inadequate bone formation, including osteoporosis.
Phytotherapy Research 10/2009; 24(4):571-6. · 2.09 Impact Factor
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Clinical and Experimental Optometry 09/2009; 92(6):500-2. · 1.05 Impact Factor
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[show abstract]
[hide abstract]
ABSTRACT: The present study aimed to construct a 1.5X hepatitis B virus (HBV) replication system in vitro that could generate high level of HBV viruses. This system would help compare the replication capacity among the virus strains associated with high and low risk of hepatocellular carcinoma (HCC). Four strains of HBV were isolated from two HCC patients and two HBV carriers. After molecular cloning, four corresponding constructs named as HBV-1.5Xs were generated. Each of them has one and a half copies of HBV 3.2kb genome, a 5'-end redundant sequence of 1.1kb to nt715 and a 3'-end redundant sequence of 500bp to nt2325 that situated after the poly (A) sequence. The HepG2 cells were transfected with the HBV-1.5Xs, and the levels of HBsAg, HBeAg and viral DNA were then detected in both the supernatant and the cells. After 24h and 48h of transfection, a high OD value of HBsAg of 3.5 was observed in the supernatant and also in some of the diluted cell lysate samples. The HBeAg level was relatively low in all strain samples of HBV. The log(10) values of viral loads were also determined with the cell lysate having a higher value (10-11 per ml) than that of the supernatant (6-7 per ml). The results showed that the novel HBV-1.5X system was capable to generate high level of HBV in a consistent manner. However, no significant difference was found among the replication capacities among these strains in vitro. The HBV-1.5X system may be a useful platform that assists the establishment of stable cell lines and transgenic mice for the investigation of viral pathogenesis, particularly for the various strains of HBV.
Journal of virological methods 09/2009; 159(2):135-40. · 2.13 Impact Factor
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Ming Li,
Jide Wang,
Samuel S M Ng, Chu-Yan Chan,
Ming-Liang He,
Fang Yu,
Lihui Lai,
Chao Shi,
Yangchao Chen,
David T Yew,
Hsiang-Fu Kung,
Marie Chia-Mi Lin
[show abstract]
[hide abstract]
ABSTRACT: : Epidermal growth factor (EGF) signaling plays a pivotal role in gliomagenesis. The authors previously demonstrated that adenosine diphospate-ribosylation factor 6 (ARF6), a member of the Ras-related small guanosine-5'-triphospate-binding protein family, is required for EFA6A-induced glioma cell migration and invasion. However, the role of ARF6 in EGF signaling is unknown.
: The authors analyzed messenger RNA (mRNA) levels of ARF6 and EGF receptor (EGFR) in 16 high-grade glioma samples and in 6 low-grade glioma samples by reverse transcriptase-polymerase chain reaction analysis. To determine whether EGF induces ARF6 expression in human glioblastoma U87 cells through transcriptional regulation and EGFR activation, the levels of ARF6 were assayed in EGF-treated U87 cells that were preincubated with a transcriptional inhibitor (actinomycin D) and an EGFR tyrosine kinase inhibitor (PD153035), respectively. The downstream signaling of EGFR-mediated ARF6 up-regulation also was investigated using specific inhibitors of mitogen-activated protein kinase (MEK), phosphatidylinositol 3' kinase (PI3K), and Janus kinase 2. The involvement of SP1 in the downstream signaling was studied by using an SP1 inhibitor (mithramycin A). Small-interfering RNAs (siRNAs) targeting ARF6 were used to investigate the effects of ARF6 on EGF-mediated glioma cell proliferation.
: The results demonstrated that ARF6 and EGFR mRNA levels were elevated in glioma tissues. Furthermore, EGF stimulated ARF6 expression in U87 cells in a dose-dependent and time-dependant manner. This stimulation was caused by increased transcription of ARF6 and by activation of the MEK/extracellular signal-regulated kinase 1 and 2 (ERK1/2) and PI3K signaling pathways. It is noteworthy that SP1 was essential for EGF-induced ARF6 up-regulation. Finally, EGF-induced glioblastoma cell proliferation depended on ARF6, because the suppression of ARF6 by siRNA or by a dominant-negative mutant significantly inhibited EGF-induced cell proliferation.
: The results of the current study suggested that EGF-induced ARF6 expression plays a significant role in glioma cell proliferation. Cancer 2009. (c) 2009 American Cancer Society.
Cancer 08/2009; 115(21):4959-72. · 4.77 Impact Factor
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Bing Liang,
Ming-Liang He, Chu-yan Chan,
Yang-chao Chen,
Xiang-Ping Li,
Yi Li,
Dexian Zheng,
Marie C Lin,
Hsiang-Fu Kung,
Xin-Tao Shuai,
Ying Peng
[show abstract]
[hide abstract]
ABSTRACT: Combined treatment using nonviral agent-mediated enzyme/prodrug therapy and immunotherapy had been proposed as a powerful alternative method of cancer therapy. The present study was aimed to evaluate the cytotoxicity in vitro and the therapeutic efficacy in vivo when the cytosine deaminase/5-fluorocytosine (CD/5-FC) and TNF-related apoptosis-inducing ligand (TRAIL) genes were jointly used against rat C6 glioma cells. The potency of the FA-PEG-PEI used as a nonviral vector was tested in the FR-expressed C6 glioma cells and Wistar rats. The C6 glioma cells and animal model were treated by the combined application of FA-PEG-PEI/pCD/5-FC and FA-PEG-PEI/pTRAIL. The antitumor effect was evaluated by survival assays and tumor volume. This study revealed a significant increase of cytotoxicity in vitro following the combined application of FA-PEG-PEI/pCD/5-FC and FA-PEG-PEI/pTRAIL treatments in C6 glioma cells. Animal studies showed a significant growth inhibition of the C6 glioma xenografts using the combined treatment. These results demonstrated that the combined treatment generated additive cytotoxic effect in C6 glioma cells in both in vitro and in vivo conditions, and indicated that such treatment method using both enzyme/prodrug therapy and TRAIL immunotherapy might be a promising therapeutic strategy in treating glioma.
Biomaterials 06/2009; 30(23-24):4014-20. · 7.40 Impact Factor
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Guo Li,
Xiao-ai Zhang,
Hua Wang,
Xin Wang,
Chun-ling Meng, Chu-yan Chan,
David Tai Wai Yew,
Kam Sze Tsang,
Karen Li,
Sau-na Tsai,
Sai-ming Ngai,
Zhong Chao Han,
Marie Chia-mi Lin,
Ming-liang He,
Hsiang-fu Kung
[show abstract]
[hide abstract]
ABSTRACT: Umbilical cord (UC) and placenta (P) have been suggested as alternatives to bone marrow (BM) as sources of mesenchymal stem cells (MSC) for cell therapy, with both UC- and P-MSC possess immunophenotypic and functional characteristics similar to BM-MSC. However, their migration capacity, which is indispensable during tissue regeneration process, is unclear. Under defined conditions, the migration capacity of BM- and P-MSC was found 5.9- and 3.2-folds higher than that of UC-MSC, respectively. By the use of 2-DE and combined MS and MS/MS analysis, six differentially expressed proteins were identified among these MSC samples, with five of them known to be involved in cell migration as migration enhancing or inhibiting proteins. Consistent with their migration capacity, the levels of migration enhancing proteins including cathepsin B, cathepsin D and prohibitin,were significantly lower in UC-MSC when compared with those in BM- and P-MSC. For the migration inhibiting proteins such as plasminogen activator inhibitor-1 (PAI-1) and manganese superoxide dismutase, higher expression was found in the UC-MSC. We also showed that the overexpression of the PAI-1 impaired the migration capacity of BM- and P-MSC while silencing of PAI-1 enhanced the migration capacity of UC-MSC. Our study indicates that PAI-1 and other migration-related proteins are pivotal in governing the migration capacity of MSC.
Proteomics 02/2009; 9(1):20-30. · 4.43 Impact Factor
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Zhi Li,
Ming-Liang He,
Hong Yao,
Qing-Ming Dong,
Yang-Chao Chen, Chu-Yan Chan,
Bo-Jian Zheng,
Kwok-Yung Yuen,
Ying Peng,
Qiang Sun,
Xiao Yang,
Marie C Lin,
Joseph J Y Sung,
Hsiang-Fu Kung
[show abstract]
[hide abstract]
ABSTRACT: Hepatitis B virus (HBV) infection is highly prevalent worldwide. The major challenge for current antiviral treatment is the elevated drug resistance that occurs via rapid viral mutagenesis. In this study, we developed AAV vectors to simultaneously deliver two or three shRNAs targeting different HBV-related genes. These vectors showed markedly better antiviral effects than ones that delivered a single shRNA in vitro. A dual shRNA expression vector (AAV-157i/1694i), which simultaneously expressed two shRNAs targeted the S and X genes of HBV, reduced HBsAg, HBeAg and HBV DNA levels by 87+/-4, 80.3+/-2.6 and 86.2+/- 7% respectively, eight days post-transduction. In a mouse model of prophylactic treatment, HBsAg and HBeAg were reduced to undetectable levels and the serum HBV DNA level was reduced by at least 100 fold. These results indicate that AAV-157i/1694i generates potent anti-HBV effects and that the strategy of constructing multi-shRNA expression vectors may lead to enhanced anti-HBV efficacy and overcome the evading mechanism of the virus and thus the development of drug resistance. [BMB reports 2009; 42(1): 59-64].
BMB reports 02/2009; 42(1):59-64. · 1.72 Impact Factor
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Xin Wang,
Yangchao Chen,
Quan-bin Han, Chu-yan Chan,
Hua Wang,
Zheng Liu,
Christopher Hon-ki Cheng,
David T Yew,
Marie C M Lin,
Ming-liang He,
Hong-xi Xu,
Joseph J Y Sung,
Hsiang-fu Kung
[show abstract]
[hide abstract]
ABSTRACT: Gamboge has been developed as an injectable drug for cancer treatment in China. In this study, the inhibition ratio and their IC(50) values of two derivatives from Gamboge in hepatocellular carcinoma (HCC) were determined. Proteomic approach was employed to reveal the target proteins of these two derivatives, gambogic acid (GA), and gambogenic acid (GEA). HCC cells were cultured under varied conditions with the addition of either GA or GEA. Twenty differentially expressed proteins were identified and the four most distinctly expressed proteins were further validated by Western blotting. GA and GEA revealed inhibitory effects on HCC cell proliferation. The expression of cyclin-dependent kinase 4 inhibitor A and guanine nucleotide-binding protein beta subunit 1 were upregulated by both xanthones, whilst the expression of 14-3-3 protein sigma and stathmin 1 (STMN1) were downregulated. Furthermore, overexpression of STMN1 in HCC cells decreased their sensitivity, whilst small interfering RNAs targeting STMN1 enhanced their sensitivity to GA and GEA. In conclusion, our study suggested for the first time that STMN1 might be a major target for GA and GEA in combating HCC. Further investigation may lead to a new generation of anticancer drugs exerting synergistic effect with conventional therapy, thus to promote treatment efficacy.
Proteomics 01/2009; 9(2):242-53. · 4.43 Impact Factor
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Lei Jiang,
Yangchao Chen, Chu-yan Chan,
Xin Wang,
Lin Lin,
Ming-liang He,
Marie C M Lin,
David T Yew,
Joseph J Y Sung,
Ji-Cheng Li,
Hsiang-fu Kung
[show abstract]
[hide abstract]
ABSTRACT: Transforming growth factor-beta (TGF-beta) inducible early gene 1 (TIEG1) is known to induce apoptosis in TGF-beta sensitive pancreatic cancer cells, yet its effect on TGF-beta resistant cancer cells remains unclear. In this study, TIEG1 was found to induce apoptosis in TGF-beta resistant cancer cells and concurrently enhanced gemcitabine chemosensitivity. Down-regulation of stathmin was noted to associate with TIEG1 expression, whilst ectopic overexpression of stathmin prevented TIEG1 mediated growth inhibition of tumor cells. Small interfering RNAs targeting stathmin inhibited pancreatic cancer cell growth. These suggest that stathmin is a downstream target of TIEG1.
Cancer letters 11/2008; 274(1):101-8. · 4.86 Impact Factor
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Ming Li,
Jide Wang,
Samuel S M Ng, Chu-Yan Chan,
Amy C Chen,
Hong Ping Xia,
David T Yew,
Benjamin C Y Wong,
Zhu Chen,
Hsiang-Fu Kung,
Marie Chia-Mi Lin
[show abstract]
[hide abstract]
ABSTRACT: Four-and-a-half-LIM protein 2 (FHL2) is a member of FHL protein family, which plays a crucial role in regulating gene expression, cell survival, and migration. Although its function in oncogenesis appears to be tumor type-specific, its roles in glioma formation and development are yet to be elucidated. In the present study, we demonstrated that the mRNA level of FHL2 was elevated in both low- and high-grade glioma samples. Overexpression of FHL2 stimulated the proliferation, anchorage-independent growth, and migration of human glioblastoma cells. Conversely, FHL2 knockdown by short hairpin RNA (shRNA-FHL2) inhibited glioblastoma cell proliferation and migration. Overexpression of FHL2 increased the tumorigenicity of glioblastoma cells in nude mice and decreased the mRNA levels of p53 and its downstream proapoptotic genes, including p21, Bcl2-associated protein X (Bax), and p53-upregulated modulator of apoptosis. It also enhanced the promoter activities of activator protein-1 (AP-1), human telomerase reverse transcriptase, and survivin genes. Together, these results provide the first evidence that FHL2 contributes to glioma carcinogenesis.
Glia 08/2008; 56(12):1328-38. · 4.82 Impact Factor
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Zhi Li,
Hong Yao,
Yan Ma,
Qingming Dong,
Yangchao Chen,
Ying Peng,
Bo-jian Zheng,
Jian-dong Huang, Chu-yan Chan,
Marie C Lin,
Joseph J Sung,
Kwok Yun Yuen,
Hsiang-fu Kung,
Ming-Liang He
[show abstract]
[hide abstract]
ABSTRACT: Interferon-alpha2 (IFNalpha2) is routinely used for anti-hepatitis B virus (HBV) treatment. However, the therapeutic efficiency is unsatisfactory, particularly in East Asia. Such inefficiency might be a result of the short half-life, relatively low local concentration and strong side-effects of interferons. Frequent and repeated injection is also a big burden for patients. In the present study, a single dose of vector-delivered IFNalpha1 was tested for its anti-HBV effects.
Adeno-associated viral vector (AAV-IFNalpha1) was generated to deliver the IFNalpha1 gene into hepatocytes. IFNalpha1, hepatitis B surface (HBsAg) and e (HBeAg) antigens were measured by enzyme-linked immunosorbent assay and/or western blotting. The level of viral DNA was measured by quantitative real-time polymerase chain reaction.
AAV-IFNalpha1 effectively transduced HBV-producing cells (HepAD38) and mouse hepatocytes, where IFNalpha1 was expressed in a stable manner. Both intracellular and extracellular HBsAg and HBeAg were significantly reduced in vitro. In the HBV-producing mice, the concentration of IFNalpha1 in the liver was eight-fold higher than that in plasma. Compared with control groups, HBeAg/HBsAg antigen levels were reduced by more than ten-fold from day 1-5, and dropped to an undetectable level on day 9 in the AAV-IFNalpha1 group. Concurrently, the level of viral DNA decreased over 30-fold for several weeks.
A single dose administration of AAV-IFNalpha1 viral vector displayed prolonged transgene expression and superior antiviral effects both in vitro and in vivo. Therefore, the use of AAV-IFNalpha1 might be a potential alternative strategy for anti-HBV therapy.
The Journal of Gene Medicine 07/2008; 10(6):619-27. · 2.48 Impact Factor
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[show abstract]
[hide abstract]
ABSTRACT: A great challenge for gene therapy is to develop a high efficient gene delivery system with low toxicity. Nonviral vectors are still attractive although the current agents displayed some disadvantages (i.e., low transfection efficiency, high toxicity). To overcome the high toxicity of poly(ethylene imine) (PEI) and low transfection efficiency of PEGylated PEI (PEG-PEI), we linked a cell specific target molecule folate (FA) on poly(ethylene glycol) (PEG) and then grafted the FA-PEG onto hyperbranched PEI 25kDa. The FA-PEG- grafted-hyperbranched-PEI (FA-PEG-PEI) effectively condensed plasmid DNA (pDNA) into nanoparticles with positive surface charge under a suitable N/P ratio. Tested in deferent cell lines (i.e., HEK 293T, glioma C6 and hepatoma HepG2 cells), no significant cytotoxicity of FA-PEG-PEI was added to PEG-PEI. More importantly, significant transfection efficiency was exhibited in FA-targeted cells. Reporter assay showed that FA-PEG-PEI/pDNA complexes had significantly higher transgene activity than that of PEI/pDNA in folate-receptor (FR) positive (HEK 293T and C6) cells but not FR-negative (HepG2) cells. These results indicated that FA-PEG-PEI might be a promising candidate for gene delivery with the characteristics of good biocompatibility, potential biodegradability, and relatively high gene transfection efficiency.
Biochemical and Biophysical Research Communications 04/2008; 367(4):874-80. · 2.48 Impact Factor
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[show abstract]
[hide abstract]
ABSTRACT: Hypoxia is a consistent challenge for aquatic animals. It is a pressing environmental problem; hypoxia can cause cranial edema and ovarium dysfunction in fish. Although several studies have reported the effect of hypoxic insult to the visual system, the hypoxic effect on perinatal animals and in particular their offspring has yet to be elucidated. In this study, activated caspase-3 activity was investigated using immunohistochemistry in order to examine the perinatal hypoxic damage in offspring fish. Offspring were divided into groups based on different time points of sacrifice. This allowed assessment of ocular development for different age groups. The results indicated that perinatal hypoxia induced ocular developmental defects in the offspring. The defects took the form of trabecular cell death and fibre degeneration, corneal thinning and lens fibre derangement. A concomitant change in intraocular pressure was recorded by tonometer in the experimental animals compared with the controls. Further investigation should be initiated to develop strategies to prevent developmental disability due to perinatal hypoxia and to increase survivability of the offspring.
Journal of Reproduction and Development 01/2008; 53(6):1159-67. · 1.46 Impact Factor
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12/2007: pages 61-86;
