10 results on '"Xiang, Li-Jun"'
Search Results
2. A specific HeLa cell-labelled and lysosome-targeted upconversion fluorescent probe: PEG-modified Sr2YbF7:Tm3+ .
- Author
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Xiang, Li-Jun, Zhang, Hui-Hui, Li, Hong, Kong, Lin, Zhou, Hong-Ping, Wu, Jie-Ying, Tian, Yu-Peng, Zhang, Jie, and Mao, Yi-Fu
- Published
- 2017
- Full Text
- View/download PDF
3. The Anti-Scar Effects of Basic Fibroblast Growth Factor on the Wound Repair In Vitro and In Vivo.
- Author
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Shi, Hong-Xue, Lin, Cai, Lin, Bei-Bei, Wang, Zhou-Guang, Zhang, Hong-Yu, Wu, Fen-Zan, Cheng, Yi, Xiang, Li-Jun, Guo, Di-Jiong, Luo, Xu, Zhang, Guo-You, Fu, Xiao-Bing, Bellusci, Saverio, Li, Xiao-Kun, and Xiao, Jian
- Subjects
HYPERTROPHIC scars ,FIBROBLAST growth factors ,WOUND healing ,DRUG efficacy ,EXTRACELLULAR matrix ,TRANSFORMING growth factors ,GENE expression ,ANIMAL models in research ,THERAPEUTICS - Abstract
Hypertrophic scars (HTS) and keloids are challenging problems. Their pathogenesis results from an overproduction of fibroblasts and excessive deposition of collagen. Studies suggest a possible anti-scarring effect of basic fibroblast growth factor (bFGF) during wound healing, but the precise mechanisms of bFGF are still unclear. In view of this, we investigated the therapeutic effects of bFGF on HTS animal model as well as human scar fibroblasts (HSF) model. We show that bFGF promoted wound healing and reduced the area of flattened non-pathological scars in rat skin wounds and HTS in the rabbit ear. We provide evidence of a new therapeutic strategy: bFGF administration for the treatment of HTS. The scar elevation index (SEI) and epidermal thickness index (ETI) was also significantly reduced. Histological reveal that bFGF exhibited significant amelioration of the collagen tissue. bFGF regulated extracellular matrix (ECM) synthesis and degradation via interference in the collagen distribution, the α-smooth muscle actin (α-SMA) and transforming growth factor-1 (TGF-β1) expression. In addition, bFGF reduced scarring and promoted wound healing by inhibiting TGFβ1/SMAD-dependent pathway. The levels of fibronectin (FN), tissue inhibitor of metalloproteinase-1 (TIMP-1) collagen I, and collagen III were evidently decreased, and matrix metalloproteinase-1 (MMP-1) and apoptosis cells were markedly increased. These results suggest that bFGF possesses favorable therapeutic effects on hypertrophic scars in vitro and in vivo, which may be an effective cure for human hypertrophic scars. [ABSTRACT FROM AUTHOR]
- Published
- 2013
- Full Text
- View/download PDF
4. Fibroblast Growth Factors Stimulate Hair Growth through [beta]-Catenin and Shh Expression in C57BL/6 Mice.
- Author
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Lin, Wei-Hong, Xiang, Li-Jun, Shi, Hong-Xue, Zhang, Jian, Jiang, Li-Ping, Cai, Ping-Tao, Lin, Zhen-Lang, Lin, Bei-Bei, Huang, Yan, Zhang, Hai-Lin, Fu, Xiao-Bing, Guo, Ding-Jiong, Li, Xiao-Kun, Wang, Xiao-Jie, and Xiao, Jian
- Published
- 2015
- Full Text
- View/download PDF
5. The Anti-Scar Effects of Basic Fibroblast Growth Factor on the Wound Repair In Vitro and In Vivo.
- Author
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Shi, Hong-Xue, Lin, Cai, Lin, Bei-Bei, Wang, Zhou-Guang, Zhang, Hong-Yu, Wu, Fen-Zan, Cheng, Yi, Xiang, Li-Jun, Guo, Di-Jiong, Luo, Xu, Zhang, Guo-You, Fu, Xiao-Bing, Bellusci, Saverio, Li, Xiao-Kun, and Xiao, Jian
- Subjects
- *
HYPERTROPHIC scars , *FIBROBLAST growth factors , *WOUND healing , *DRUG efficacy , *EXTRACELLULAR matrix , *TRANSFORMING growth factors , *GENE expression , *ANIMAL models in research , *THERAPEUTICS - Abstract
Hypertrophic scars (HTS) and keloids are challenging problems. Their pathogenesis results from an overproduction of fibroblasts and excessive deposition of collagen. Studies suggest a possible anti-scarring effect of basic fibroblast growth factor (bFGF) during wound healing, but the precise mechanisms of bFGF are still unclear. In view of this, we investigated the therapeutic effects of bFGF on HTS animal model as well as human scar fibroblasts (HSF) model. We show that bFGF promoted wound healing and reduced the area of flattened non-pathological scars in rat skin wounds and HTS in the rabbit ear. We provide evidence of a new therapeutic strategy: bFGF administration for the treatment of HTS. The scar elevation index (SEI) and epidermal thickness index (ETI) was also significantly reduced. Histological reveal that bFGF exhibited significant amelioration of the collagen tissue. bFGF regulated extracellular matrix (ECM) synthesis and degradation via interference in the collagen distribution, the α-smooth muscle actin (α-SMA) and transforming growth factor-1 (TGF-β1) expression. In addition, bFGF reduced scarring and promoted wound healing by inhibiting TGFβ1/SMAD-dependent pathway. The levels of fibronectin (FN), tissue inhibitor of metalloproteinase-1 (TIMP-1) collagen I, and collagen III were evidently decreased, and matrix metalloproteinase-1 (MMP-1) and apoptosis cells were markedly increased. These results suggest that bFGF possesses favorable therapeutic effects on hypertrophic scars in vitro and in vivo, which may be an effective cure for human hypertrophic scars. [ABSTRACT FROM AUTHOR]
- Published
- 2013
- Full Text
- View/download PDF
6. Circ_0003356 suppresses gastric cancer growth through targeting the miR-668-3p/SOCS3 axis.
- Author
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Li WD, Wang HT, Huang YM, Cheng BH, Xiang LJ, Zhou XH, Deng QY, Guo ZG, Yang ZF, Guan ZF, and Wang Y
- Abstract
Background: Circular RNAs (circRNAs) have attracted extensive attention as therapeutic targets in gastric cancer (GC). Circ_0003356 is known to be downregulated in GC tissues, but its cellular function and mechanisms remain undefined., Aim: To investigate the role of circ_0003356 in GC at the molecular and cellular level., Methods: Circ_0003356, miR-668-3p, and SOCS3 expression were assessed via quantitative real time-polymerase chain reaction (qRT-PCR). Wound healing, EdU, CCK-8, flow cytometry and transwell assays were used to analyze the migration, proliferation, viability, apoptosis and invasion of GC cells. The subcellular localization of circ_0003356 was monitored using fluorescence in situ hybridization. The interaction of circ_0003356 with miR-668-3p was confirmed using RIP-qRT-PCR, RNA pull-down, and dual luciferase reporter assays. We observed protein levels of genes via western blot. We injected AGS cells into the upper back of mice and performed immunohistochemistry staining for examining E-cadherin, N-cadherin, Ki67, and SOCS3 expressions. TUNEL staining was performed for the assessment of apoptosis in mouse tumor tissues., Results: Circ_0003356 and SOCS3 expression was downregulated in GC cells, whilst miR-668-3p was upregulated. Exogenous circ_0003356 expression and miR-668-3p silencing suppressed the migration, viability, proliferation, epithelial to mesenchy-mal transition (EMT) and invasion of GC cells and enhanced apoptosis. Circ_0003356 overexpression impaired tumor growth in xenograft mice. Targeting of miR-668-3p by circ_0003356 was confirmed through binding assays and SOCS3 was identified as a downstream target of miR-668-3p. The impacts of circ_0003356 on cell proliferation, apoptosis, migration, invasion and EMT were reversed by miR-668-3p up-regulation or SOCS3 down-regulation in GC cells., Conclusion: Circ_0003356 impaired GC development through its interaction with the miR-668-3p/SOCS3 axis., Competing Interests: Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article., (©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.)
- Published
- 2023
- Full Text
- View/download PDF
7. A water-soluble, upconverting Sr 2 Yb 0.3 Gd 0.7 F 7 :Er 3+ /Tm 3+ @PSI oAm bio-probe for in vivo trimodality imaging.
- Author
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Xiang LJ, Zhu XJ, Zhang HH, Yang L, Deng KX, Liu Y, Ye MS, Hu L, Yang XY, and Zhou HP
- Abstract
Multi-modality in vivo bioimaging has great renown for offering more comprehensive information in medical diagnosis and research. Incorporating different bioimaging capabilities into one biocompatible nanoprobe requires an elegant structural design. Considering optical and magnetic properties, X-ray absorption ability, and clinical safety, we prepared a water-soluble and upconverting PSIoAm-modified Sr2Yb0.3Gd0.7F7:Er3+/Tm3+ bio-probe that not only had high photostability and excellent cell membrane permeability, but could also distinguish the four types of cancer cells and normal cells tested within the scope of our study. What's more, it could realize the in vivo trimodality imaging of upconversion fluorescence, X-ray computed tomography and magnetic resonance. The histological analysis of visceral sections further demonstrated that the multifunctional bio-probe was highly safe, which could be applied to clinical diagnosis.
- Published
- 2018
- Full Text
- View/download PDF
8. A specific HeLa cell-labelled and lysosome-targeted upconversion fluorescent probe: PEG-modified Sr 2 YbF 7 :Tm 3+ .
- Author
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Xiang LJ, Zhang HH, Li H, Kong L, Zhou HP, Wu JY, Tian YP, Zhang J, and Mao YF
- Subjects
- Animals, Fibroblasts, HeLa Cells, Humans, Mice, Microscopy, Confocal, Microscopy, Fluorescence, Nanoparticles, Organelles, Ytterbium, Fluorescent Dyes, Lysosomes
- Abstract
In this study, water-soluble PEG-modified Sr
2 YbF7 :Tm3+ was prepared conveniently by a one-pot solvothermal method, where the molar ratio of Sr2+ to Yb3+ was controlled between 3 : 2 and 1 : 1. The optimum red-light emission at 677-699 nm was modulated via 0.7% Tm3+ doped under irradiation at 980 nm. Interestingly, biological experimental results showed that the PEG-modified Sr2 YbF7 :Tm3+ with low toxicity, excellent cell membrane permeability and high photostability can not only distinguish HeLa cells from mouse embryonic fibroblasts but also target the subcellular organelle lysosome in HeLa cells; therefore it can be anticipated that the as-prepared material would be a potential tool for cancer diagnosis.- Published
- 2017
- Full Text
- View/download PDF
9. Dihydromyricetin-mediated inhibition of the Notch1 pathway induces apoptosis in QGY7701 and HepG2 hepatoma cells.
- Author
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Lu CJ, He YF, Yuan WZ, Xiang LJ, Zhang J, Liang YR, Duan J, He YH, and Li MY
- Subjects
- Antineoplastic Agents, Phytogenic therapeutic use, Apoptosis drug effects, Carcinoma, Hepatocellular pathology, Cell Proliferation drug effects, Disease Progression, Down-Regulation, Flavonols therapeutic use, Flow Cytometry, Hep G2 Cells, Humans, Liver Neoplasms pathology, Proto-Oncogene Proteins c-bcl-2 metabolism, RNA Interference, RNA, Small Interfering metabolism, Receptor, Notch1 genetics, Up-Regulation, bcl-2-Associated X Protein metabolism, Antineoplastic Agents, Phytogenic pharmacology, Carcinoma, Hepatocellular drug therapy, Flavonols pharmacology, Liver Neoplasms drug therapy, Receptor, Notch1 metabolism, Signal Transduction drug effects
- Abstract
Aim: To investigate whether Dihydromyricetin (DHM) inhibits cell proliferation and promotes apoptosis by downregulating Notch1 expression., Methods: The correlation between Notch1 and Hes1 (a Notch1 target molecule) expression in hepatoma samples was confirmed by qRT-PCR. In addition, MTT assays, flow cytometry and TUNEL analysis showed that DHM possessed strong anti-tumor properties, evidenced not only by reduced cell proliferation but also by enhanced apoptosis in QGY7701 and HepG2 hepatocellular carcinoma (HCC) cells. The expressions of Notch1, Hes1, Bcl-2 and Bax were determined by Western blot., Results: Among the tested samples ( n = 64), the expression levels of Notch1 (75% of patients) and Hes1 (79.7% of patients) mRNA in tumor tissues were higher than in the normal liver tissues. There was a negative correlation between the expression of Notch1 and the degree of differentiation and positively correlated with the Alpha Fetal Protein concentration. The viability of HCC cells treated with DHM was significantly inhibited in a dose and time-dependent manner. Apoptosis was induced in HepG2 and QGY7701 cell lines following 24 h of DHM treatment. After treatment with DHM, the protein expression of Notch1 was downregulated, the apoptosis-related protein Bax was upregulated and Bcl2 was downregulated. Notch1 siRNA further enhanced the anti-tumor properties of DHM., Conclusion: Notch1 is involved in the development of HCC and DHM inhibits cell proliferation and promotes apoptosis by down-regulating the expression of Notch1., Competing Interests: Conflict-of-interest statement: The authors deny any conflict of interest.
- Published
- 2017
- Full Text
- View/download PDF
10. The anti-scar effects of basic fibroblast growth factor on the wound repair in vitro and in vivo.
- Author
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Shi HX, Lin C, Lin BB, Wang ZG, Zhang HY, Wu FZ, Cheng Y, Xiang LJ, Guo DJ, Luo X, Zhang GY, Fu XB, Bellusci S, Li XK, and Xiao J
- Subjects
- Actins metabolism, Animals, Antigens, CD metabolism, Antigens, Differentiation, Myelomonocytic metabolism, Apoptosis drug effects, Cicatrix, Hypertrophic drug therapy, Collagen Type I biosynthesis, Collagen Type III biosynthesis, Fibroblasts drug effects, Fibroblasts metabolism, Gene Expression, Humans, Immunohistochemistry, Male, Models, Animal, Proliferating Cell Nuclear Antigen metabolism, Rabbits, Rats, Signal Transduction drug effects, Transforming Growth Factor beta1 metabolism, Fibroblast Growth Factor 2 pharmacology, Wound Healing drug effects, Wound Healing physiology
- Abstract
Hypertrophic scars (HTS) and keloids are challenging problems. Their pathogenesis results from an overproduction of fibroblasts and excessive deposition of collagen. Studies suggest a possible anti-scarring effect of basic fibroblast growth factor (bFGF) during wound healing, but the precise mechanisms of bFGF are still unclear. In view of this, we investigated the therapeutic effects of bFGF on HTS animal model as well as human scar fibroblasts (HSF) model. We show that bFGF promoted wound healing and reduced the area of flattened non-pathological scars in rat skin wounds and HTS in the rabbit ear. We provide evidence of a new therapeutic strategy: bFGF administration for the treatment of HTS. The scar elevation index (SEI) and epidermal thickness index (ETI) was also significantly reduced. Histological reveal that bFGF exhibited significant amelioration of the collagen tissue. bFGF regulated extracellular matrix (ECM) synthesis and degradation via interference in the collagen distribution, the α-smooth muscle actin (α-SMA) and transforming growth factor-1 (TGF-β1) expression. In addition, bFGF reduced scarring and promoted wound healing by inhibiting TGFβ1/SMAD-dependent pathway. The levels of fibronectin (FN), tissue inhibitor of metalloproteinase-1 (TIMP-1) collagen I, and collagen III were evidently decreased, and matrix metalloproteinase-1 (MMP-1) and apoptosis cells were markedly increased. These results suggest that bFGF possesses favorable therapeutic effects on hypertrophic scars in vitro and in vivo, which may be an effective cure for human hypertrophic scars.
- Published
- 2013
- Full Text
- View/download PDF
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