Search

Your search keyword '"Zhouguang Wu"' showing total 12 results
Start Over Author "Zhouguang Wu"
12 results on '"Zhouguang Wu"'

1. Management of traumatic duodenal rupture in children-case series

Author

Zhen Cheng, Yuelan Zheng, Jiahui Gao, Zhouguang Wu, Qi Feng, and Bin Wang

Subjects
Children, Duodenal rupture, Diagnosis, Surgery, Postoperative management, Pediatrics, RJ1-570
Abstract

Abstract Background Traumatic duodenal rupture is rare which accounts for only 2–10% of all Blunt abdominal trauma. The purpose of this study was to investigate the experience of diagnosis and treatment of traumatic duodenal rupture in children. Methods This was a retrospective case series study. Clinical data were collected from three children suffering from a traumatic duodenal rupture who received surgical treatment in our hospital from January 2013 to January 2023. Demographic characteristics, trauma mechanism, physical examination, auxiliary examination, operation timing and plan, postoperative management and follow-up of included patients were described. Summarize the importance of early diagnosis and treatment of this type of injury. Results Three children (1 male and 2 females) with duodenal rupture due to traumatic abdominal injury were included in the study, with average age of 8.2 years (range 2.75–13.25 years). Among them, One child was injured by heavy objects. The other two children had lumbar fracture and seat belt sign. All three patients underwent emergency operation within 24 h, and recovered well after surgery. No related complications seen during follow-up. Conclusions Duodenal rupture is a rare but fatal disease. Early identification and active abdominal exploration can reduce the incidence of related complications and mortality in children with blunt abdominal injury, especially those with seat belt sign. Simultaneously, the standardized postoperative management is significant for the cure of children.

Published
2024
Full Text
View/download PDF

2. Hsa_circ_0009096/miR-370-3p modulates hepatic stellate cell proliferation and fibrosis during biliary atresia pathogenesis

Author

Zhouguang Wu, Bin Wang, Siqi Chen, Taoyan Zuo, Wenjie Zhang, Zhen Cheng, Jingru Fu, and Jiafeng Gong

Subjects
Hsa_circ_0009096, miR-370-3p, HSCs, Hepatic fibrosis, BA, TGFBR2, Medicine, Biology (General), QH301-705.5
Abstract

Background Hepatic stellate cell (HSC) activation and hepatic fibrosis mediated biliary atresia (BA) development, but the underlying molecular mechanisms are poorly understood. This study aimed to investigate the roles of circRNA hsa_circ_0009096 in the regulation of HSC proliferation and hepatic fibrosis. Methods A cellular hepatic fibrosis model was established by treating LX-2 cells with transforming growth factor β (TGF-β1). RNaseR and actinomycin D assays were performed to detect hsa_circ_0009096 stability. Expression of hsa_circ_0009096, miR-370-3p, and target genes was detected using reverse transcription-qPCR. Direct binding of hsa_circ_0009096 to miR-370-3p was validated using dual luciferase reporter assay. Cell cycle progression and apoptosis of LX-2 cells were assessed using flow cytometry. The alpha-smooth muscle actin (α-SMA), collagen 1A1 (COL1A1), and TGF beta receptor 2 (TGFBR2) protein levels in LX-2 cells were analyzed using immunocytochemistry and western blotting. Results Hsa_circ_0009096 exhibited more resistance to RNase R and actinomycinD digestion than UTRN mRNA. Hsa_circ_0009096 expression increased significantly in LX-2 cells treated with TGF-β1, accompanied by elevated α-SMA and COL1A1 expression. Hsa_circ_0009096 siRNAs effectively promoted miR-370-3p and suppressed TGFBR2 expression in LX-2 cells, mediated by direct association of hsa_circ_0009096 with miR-370-3p. Hsa_circ_0009096 siRNA interfered with the cell cycle progression, promoted apoptosis, and reduced α-SMA and COL1A1 expression in LX-2 cells treated with TGF-β1. MiR-370-3p inhibitors mitigated the alterations in cell cycle progression, apoptosis, and α-SMA, COL1A1, and TGFBR2 expression in LX-2 cells caused by hsa_circ_0009096 siRNA. In conclusion, hsa_circ_0009096 promoted HSC proliferation and hepatic fibrosis during BA pathogenesis by accelerating TGFBR2 expression by sponging miR-370-3p.

Published
2024
Full Text
View/download PDF

4. Downregulation of microRNA-145 may contribute to liver fibrosis in biliary atresia by targeting ADD3.

Author

Yongqin Ye, Zhihan Li, Qi Feng, Zimin Chen, Zhouguang Wu, Jianyao Wang, Xiaoshuo Ye, Dahao Zhang, Lei Liu, Wei Gao, Lihui Zhang, and Bin Wang

Subjects
Medicine, Science
Abstract

Biliary atresia (BA) is a pediatric liver disease characterized by fibro-obliteration and obstruction of the extrahepatic biliary system, that invariably leads to cirrhosis and even death, if left untreated for extended time. However, its pathology and etiology still remained unknown. In this study, we tested the expression of adducin 3 (ADD3), the gene identified as a susceptibility gene in BA by GWAS, and uncovered its upstream regulatory microRNA in the pathogenesis of BA.In this study, 14 infants with BA and 14 infants with choledochal cyst (CC) were enrolled as experimental group and control group, respectively. ADD3 and microRNA-145 (miR-145) expression profiles in liver tissues of BA and CC were determined using qPCR. Luciferase reporter assay was performed to verify the direct interaction between miR-145-5p and ADD3 3' Untranslated Regions (3'UTR). The Lentiviral vectors containing miR-145, miR-145-3p inhibitor, miR-145-5p inhibitor, empty vector were transfected into human hepatic stellate cell line (LX-2) to determine the functional effect of miR-145 on ADD3 expression at both mRNA and protein level.MiR-145 was shown to be down-regulated in liver tissues of infants with BA compared to CC (p = 0.0267). ADD3, verified as a target of miR-145-5p, was shown to be overexpressed in infants with BA at the mRNA level (p = 0.0118). Transfection of lentiviruses containing miR-145 into LX-2 cells decreased the expression of ADD3 at both mRNA and protein level compared to negative control group, and suppressed the expression of p-Akt at protein level.Our study has shown that overexpressed ADD3 and downregulated miR-145 were detected in BA liver tissues. MiR-145-5p was confirmed to target ADD3 by luciferase reporter assay. The downregulation of miR-145 may contribute to liver fibrosis in BA by upregulating the expression of ADD3.

Published
2017
Full Text
View/download PDF

8. Aminoacylase 1 (ACY-1) Mediates the Proliferation and Migration of Neuroblastoma Cells in Humans Through the ERK/Transforming Growth Factor β (TGF-β) Signaling Pathways

Author

Jun Sun, Zhouguang Wu, Bin Wang, Jiahui Gao, and Zimin Chen

Subjects
MAPK/ERK pathway, Canavan Disease, MAP Kinase Signaling System, education, Apoptosis, 030204 cardiovascular system & hematology, Transfection, Amidohydrolases, Flow cytometry, Neuroblastoma, 03 medical and health sciences, 0302 clinical medicine, Lab/In Vitro Research, Cell Movement, Transforming Growth Factor beta, Cell Line, Tumor, medicine, Humans, Calcium Signaling, Cell Proliferation, medicine.diagnostic_test, Chemistry, General Medicine, Cell biology, Gene Expression Regulation, Neoplastic, Blot, Cell culture, Gene Knockdown Techniques, 030220 oncology & carcinogenesis, Signal transduction, Proto-Oncogene Proteins c-akt, Signal Transduction, Transforming growth factor
Abstract

BACKGROUND Aminoacylase 1 (ACY-1) is a cytosolic enzyme that catalyzes amino acid deacylation and has been reported to participate in various human diseases. However, the role and mechanism of ACY-1 in neuroblastoma (NB) are not completely understood. The aim of this study was to elucidate the role of ACY-1 in NB. MATERIAL AND METHODS Overexpression and knockdown of ACY-1 in human NB cells were performed, and the transfection efficiency was assessed through fluorescence microscopy, real-time PCR, and western blotting. The effect of ACY-1 on tumorigenesis and metastasis was determined by cell counting, colony formation, wound healing, flow cytometry, and transwell invasion assays in vitro, and the signaling pathway was examined using western blotting. RESULTS ACY-1 overexpression inhibited proliferation and induced apoptosis in human NB cells. ACY-1 inhibited the colony formation ability, migration, and invasion of SH-SY5Y cell lines. Moreover, the ERK1/2 and TGF-ß1 signaling pathways were more active when ACY-1 was overexpressed in NB cells. However, the knockdown of ACY-1 in SH-SY5Y cell lines showed the opposite effects. CONCLUSIONS ACY-1 regulates the proliferation, migration, and invasion of human NB cells through the ERK1/2 and TGF-ß1 signaling pathways, implying that ACY-1 may serve as a therapeutic target for patients with NB.

Published
2020
Full Text
View/download PDF

9. Suppressing microRNA-29c promotes biliary atresia-related fibrosis by targeting DNMT3A and DNMT3B

Author

Hao Cheng, Yongqin Ye, Qi Feng, Yue-lan Zheng, Jian-yao Wang, Jun Yao, Bin Wang, Zimin Chen, Zhouguang Wu, and Hong-yan Zhang

Subjects
0301 basic medicine, Epithelial-Mesenchymal Transition, Short Report, Vimentin, MiR-29c, Biochemistry, DNA Methyltransferase 3A, 03 medical and health sciences, 0302 clinical medicine, Downregulation and upregulation, Fibrosis, medicine, Humans, DNA (Cytosine-5-)-Methyltransferases, Epithelial–mesenchymal transition, lcsh:QH573-671, Molecular Biology, biology, lcsh:Cytology, Chemistry, Infant, Cell Biology, Transfection, medicine.disease, Molecular medicine, Blot, MicroRNAs, 030104 developmental biology, Gene Expression Regulation, Lipofectamine, 030220 oncology & carcinogenesis, embryonic structures, Cancer research, biology.protein, DNMT3A, DNMT3B, Biliary atresia
Abstract

This study was designed to investigate the potential role of microRNA-29c (miR-29c) in biliary atresia-related fibrosis. The expression of miR-29c was determined in 15 pairs of peripheral blood samples from infants with biliary atresia (BA) and infants with non-BA neonatal cholestasis using quantitative real-time PCR. EMT was established by induction with TGF-β1 in HIBEpiC cells. MiR-29c was inhibited by lipofectamine transfection. The expressions of proteins related to epithelial–mesenchymal transition (EMT), i.e., E-cadherin, N-cadherin and vimentin, were determined using quantitative real-time PCR and western blotting. Direct interaction between miR-29c and DNMT3A and DNMT3B was identified using a luciferase reporter assay. The expressions of DNMT3A and DNMT3B were suppressed by treatment with SGI-1027. Patients with BA showed significantly lower miR-29c levels in peripheral blood samples than the control subjects. In vitro, TGF-β1-induced EMT significantly decreased the expression of miR-29c. Downregulation of miR-29c had a promotional effect on BA-related fibrosis in HIBEpiC cells, as confirmed by the decrease in E-cadherin and increase in N-cadherin and vimentin levels. MiR-29c was found to target the 3’UTR of DNMT3A and DNMT3B and inhibit their expression. Suppression of DNMT3A and DNMT3B reversed the effects of miR-29c downregulation on BA-related fibrosis in HIBEpiC cells. These data suggest that BA-related fibrosis is closely associated with the occurrence of EMT in HIBEpiC cells. MiR-29c might be a candidate for alleviating BA-related fibrosis by targeting DNMT3A and DNMT3B.

Published
2019
Full Text
View/download PDF

11. Downregulation of microRNA-145 may contribute to liver fibrosis in biliary atresia by targeting ADD3

Author

Lei Liu, Zimin Chen, Zhihan Li, Dahao Zhang, Lihui Zhang, Qi Feng, Jian-yao Wang, Bin Wang, Xiaoshuo Ye, Zhouguang Wu, Yongqin Ye, and Wei Gao

Subjects
0301 basic medicine, Liver Cirrhosis, Male, Cirrhosis, lcsh:Medicine, Gene Expression, Gastroenterology, Biochemistry, Liver disease, Binding Analysis, Gene expression, Medicine and Health Sciences, lcsh:Science, Cells, Cultured, Regulation of gene expression, Multidisciplinary, Liver Diseases, Luciferase Assay, Enzymes, Nucleic acids, Bioassays and Physiological Analysis, Liver Fibrosis, Female, Oxidoreductases, Luciferase, Cell Binding Assay, Research Article, medicine.medical_specialty, Down-Regulation, Gastroenterology and Hepatology, Biology, Transfection, Research and Analysis Methods, 03 medical and health sciences, Extraction techniques, Downregulation and upregulation, Biliary atresia, Biliary Atresia, Internal medicine, medicine, Genetics, Humans, Molecular Biology Techniques, Non-coding RNA, Molecular Biology, Chemical Characterization, Enzyme Assays, Retrospective Studies, Three prime untranslated region, lcsh:R, Biology and Life Sciences, Proteins, Infant, medicine.disease, Molecular biology, RNA extraction, Gene regulation, MicroRNAs, 030104 developmental biology, Gene Expression Regulation, Case-Control Studies, Hepatic stellate cell, Enzymology, RNA, lcsh:Q, Calmodulin-Binding Proteins, Biochemical Analysis
Abstract

Background and objectives Biliary atresia (BA) is a pediatric liver disease characterized by fibro-obliteration and obstruction of the extrahepatic biliary system, that invariably leads to cirrhosis and even death, if left untreated for extended time. However, its pathology and etiology still remained unknown. In this study, we tested the expression of adducin 3 (ADD3), the gene identified as a susceptibility gene in BA by GWAS, and uncovered its upstream regulatory microRNA in the pathogenesis of BA. Methods In this study, 14 infants with BA and 14 infants with choledochal cyst (CC) were enrolled as experimental group and control group, respectively. ADD3 and microRNA-145 (miR-145) expression profiles in liver tissues of BA and CC were determined using qPCR. Luciferase reporter assay was performed to verify the direct interaction between miR-145-5p and ADD3 3’ Untranslated Regions (3’UTR). The Lentiviral vectors containing miR-145, miR-145-3p inhibitor, miR-145-5p inhibitor, empty vector were transfected into human hepatic stellate cell line (LX-2) to determine the functional effect of miR-145 on ADD3 expression at both mRNA and protein level. Results MiR-145 was shown to be down-regulated in liver tissues of infants with BA compared to CC (p = 0.0267). ADD3, verified as a target of miR-145-5p, was shown to be overexpressed in infants with BA at the mRNA level (p = 0.0118). Transfection of lentiviruses containing miR-145 into LX-2 cells decreased the expression of ADD3 at both mRNA and protein level compared to negative control group, and suppressed the expression of p-Akt at protein level. Conclusions Our study has shown that overexpressed ADD3 and downregulated miR-145 were detected in BA liver tissues. MiR-145-5p was confirmed to target ADD3 by luciferase reporter assay. The downregulation of miR-145 may contribute to liver fibrosis in BA by upregulating the expression of ADD3.

Published
2017

12. Effect of miR-29c and miR-129-5p on epithelial-mesenchymal transition in experimental biliary atresia mouse models

Author

Zhouguang Wu, Bo Wang, Zhaohui Li, Jianping Yao, Zimin Chen, Xiaoshuo Ye, M Ye, Lei Liu, J Y Wang, and Qi Feng

Subjects
0301 basic medicine, Epithelial-Mesenchymal Transition, Primary Cell Culture, Formins, Vimentin, Transforming Growth Factor beta1, 03 medical and health sciences, Mice, Downregulation and upregulation, Western blot, Biliary Atresia, Genetics, medicine, Animals, Humans, Epithelial–mesenchymal transition, Molecular Biology, Regulation of gene expression, Keratin-19, Mice, Inbred BALB C, biology, medicine.diagnostic_test, Chemistry, Intracellular Signaling Peptides and Proteins, Rotavirus Vaccines, Epithelial Cells, General Medicine, Cadherins, Molecular biology, Disease Models, Animal, MicroRNAs, 030104 developmental biology, Real-time polymerase chain reaction, Animals, Newborn, Gene Expression Regulation, Lipofectamine, biology.protein, Female, Bile Ducts, Transforming growth factor, Signal Transduction
Abstract

Biliary atresia (BA) is a destructive bile duct disease occurring in newborn children within a few weeks after birth. In this study, the effect of miR-29c and miR-129-5p on epithelial-mesenchymal transition (EMT) in experimental BA was explored by constructing BA mouse models via Rhesus rotavirus vaccine infection. miR-29c and miR-129-5p expression was analyzed by real-time quantitative polymerase chain reaction. EMT was established by induction with transforming growth factor (TGF)-β1. miR-29c and miR-129-5p were overexpressed and inhibited, respectively, by Lipofectamine transfection. EMT-related protein (formin-like 2, FMNL2; E-cadherin; vimentin; and cytokeratin-19, CK-19) expression was analyzed by western blot and immunofluorescent assay. The results indicated that miR-29c and miR-129-5p were downregulated and upregulated in BA mice. TGF-β1 induction caused a time-dependent decrease and increase in miR-29c and miR-129-5p, respectively. Additionally, TGF-β1 induced an increase in FMNL2 and vimentin expression and a decrease in E-cadherin and CK-19 expression (P0.05). Overexpression or suppression of miRNA-29c or miR-129-5p, respectively, induced the inhibition of FMNL2 and vimentin, and promotion of E-cadherin and CK-19 expression, in the test groups compared to the non-intervention group (P0.05). However, the FMNL2, vimentin, E-cadherin, and CK- 19 expression did not differ between the control and non-intervention groups (P0.05). Thus, miR-29c upregulation or miR-129-5p downregulation effectively prevented EMT in BA by regulating the expression of EMT pathway-related proteins. Therefore, miR-29c and miR-129-5p could be utilized as therapeutic targets for BA in the future.

Published
2016

Catalog

Books, media, physical & digital resources
See catalog results