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Article ; Online: Erratum: ZEGANG FENG, FENG ZHANG & JUN CHEN (2023) Cave-dwelling Neobisiidae in South China Karst, with descriptions of twelve new species of Bisetocreagris (Pseudoscorpiones, Neobisiidae) from Guizhou Province. Zootaxa, 5395 (1): 177.

Feng, Zegang / Zhang, Feng / Chen, Jun

Zootaxa

2024 Volume 5403, Issue 5, Page(s) 597–600

Language	English
Publishing date	2024-01-24
Publishing country	New Zealand
Document type	Journal Article
ISSN	1175-5334
ISSN (online)	1175-5334
DOI	10.11646/zootaxa.5403.5.7
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Article ; Online: Salidroside ameliorated the pulmonary inflammation induced by cigarette smoke via mitigating M1 macrophage polarization by JNK/c-Jun.

Feng, Haoshen / Zhang, Dan / Yin, Yan / Kang, Jian / Zheng, Rui

Phytotherapy research : PTR

2023 Volume 37, Issue 9, Page(s) 4251–4264

Abstract: ... salidroside mitigated M1 polarization induced by CS. CSE activated the JNK/c-Jun in AMs and the M1 ... c-Jun, which indicated that salidroside mitigated the M1 polarization of AMs induced by CS via ... inhibiting JNK/c-Jun. Salidroside treatment ameliorated the pulmonary inflammation and M1 polarization of AMs ...

Abstract	Pulmonary inflammation induced by cigarette smoke (CS) promoted the development of chronic obstructive pulmonary disease (COPD), and macrophage polarization caused by CS modulated inflammatory response. Previous studies indicated that salidroside exerted therapeutic effects in COPD, but the anti-inflammatory mechanisms were not clear. This study aimed to explore the effects and mechanisms of salidroside on macrophage polarization induced by CS. Wistar rats received passively CS exposure and were treated intraperitoneally with salidroside at a low, medium or high dose. Lung tissues were stained with hematoxylin-eosin. Emphysema and inflammatory scores were evaluated by histomorphology. Lung function, cytokines, and cell differential counts in BALF were detected. The macrophage polarization was determined by immunohistochemistry in lung tissues. Alveolar macrophages (AMs) were isolated and treated with cigarette smoke extract (CSE), salidroside or inhibitors of relative pathways. The polarization status was determined by qPCR, and the protein level was detected by Western blotting. CS exposure induced emphysema and lung function deterioration. The inflammatory scores, cytokines level and neutrophils counts were elevated after CS exposure. Salidroside treatment partly ameliorated above abnormal. CS exposure activated M1 and M2 polarization of AMs in vivo and in vitro, and salidroside mitigated M1 polarization induced by CS. CSE activated the JNK/c-Jun in AMs and the M1 polarization of AMs was inhibited by the inhibitors of JNK and AP-1. Salidroside treatment deactivated the JNK/c-Jun, which indicated that salidroside mitigated the M1 polarization of AMs induced by CS via inhibiting JNK/c-Jun. Salidroside treatment ameliorated the pulmonary inflammation and M1 polarization of AMs induced by CS, and the process might be mediated by the deactivation of JNK/c-Jun.
MeSH term(s)	Rats ; Animals ; Cigarette Smoking ; Rats, Wistar ; Lung ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pneumonia ; Pulmonary Emphysema/chemically induced ; Pulmonary Emphysema/metabolism ; Macrophages/metabolism ; Cytokines/metabolism ; Emphysema/metabolism
Chemical Substances	rhodioloside (M983H6N1S9) ; Cytokines
Language	English
Publishing date	2023-05-30
Publishing country	England
Document type	Journal Article
ZDB-ID	639136-9
ISSN	1099-1573 ; 0951-418X
ISSN (online)	1099-1573
ISSN	0951-418X
DOI	10.1002/ptr.7905
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Article ; Online: ANKRD49 promotes the metastasis of NSCLC via activating JNK-ATF2/c-Jun-MMP-2/9 axis.

Sun, Jia / Hu, Jin-Rui / Liu, Chao-Feng / Li, Yuan / Wang, Wei / Fu, Rong / Guo, Min / Wang, Hai-Long / Pang, Min

BMC cancer

2023 Volume 23, Issue 1, Page(s) 1108

Abstract: ... performed to in vitro. Immunoprecipitation was performed to test the interaction of c-Jun and ATF2 ... Chromatin immunoprecipitation was conducted to assess the transcriptional regulation of ATF2/c-Jun on MMP-2/9. Moreover ... phosphorylation of JNK and then activated c-Jun and ATF2 which interact in nucleus to promote the binding of ATF2 ...

Abstract	Background: Ankyrin repeat domain 49 (ANKRD49) has been found to be highly expressed in multiple cancer including lung adenocarcinoma (LUAD) and lung squamous carcinoma (LUSC). However, the function of ANKRD49 in the pathogenesis of NSCLC still remains elusive. Previously, ANKRD49 has been demonstrated to promote the invasion and metastasis of A549 cells, a LUAD cell line, via activating the p38-ATF-2-MMP2/MMP9 pathways. Considering the heterogeneity of tumor cells, the function and mechanism of ANKRD49 in NSCLC need more NSCLC-originated cells to clarify. Methods: Real-time qPCR was employed to test ANKRD49 expression levels in nine pairs of fresh NSCLC tissues and the corresponding adjacent normal tissues. The function of ANKRD49 was investigated using overexpression and RNA interference assays in lung adenocarcinoma cell line (NCI-H1299) and lung squamous carcinoma cell line (NCI-H1703) through gelatin zymography, cell counting kit-8, colony formation, wound healing, migration and invasion assays mmunoprecipitation was performed to in vitro. Immunoprecipitation was performed to test the interaction of c-Jun and ATF2. Chromatin immunoprecipitation was conducted to assess the transcriptional regulation of ATF2/c-Jun on MMP-2/9. Moreover, the tumorigenicity of ANKRD49 was evaluated in nude mice models and the involved signal molecular was also measured by immunohistochemical method. Results: We found that the levels of ANKRD49 in cancerous tissues were higher than those in adjacent normal tissues. in vitro assay showed that ANKRD49 promoted the migration and invasion of NCI-H1299 and NCI-H1703 cells via enhancing the levels of MMP-2 and MMP-9. Furthermore, ANKRD49 elevated phosphorylation of JNK and then activated c-Jun and ATF2 which interact in nucleus to promote the binding of ATF2:c-Jun with the promoter MMP-2 or MMP-9. In vivo assay showed that ANKRD49 promoted lung metastasis of injected-NSCLC cells and the high metastatic rate was positively correlated with the high expression of ANKRD49, MMP-2, MMP-9, p-JNK, p-c-Jun and p-ATF2. Conclusion: The present study indicated that ANKRD49 accelerated the invasion and metastasis of NSCLC cells via JNK-mediated transcription activation of c-Jun and ATF2 which regulated the expression of MMP-2/MMP-9. The molecular mechanisms of ANKRD49's function is different from those found in A549 cells. The current study is a supplement and improvement to the previous research.
MeSH term(s)	Animals ; Mice ; Matrix Metalloproteinase 2/metabolism ; Matrix Metalloproteinase 9/metabolism ; Mice, Nude ; Cell Proliferation/genetics ; Cell Line, Tumor ; Carcinoma, Non-Small-Cell Lung/pathology ; Lung Neoplasms/pathology ; Carcinoma, Squamous Cell ; Adenocarcinoma of Lung
Chemical Substances	Matrix Metalloproteinase 2 (EC 3.4.24.24) ; Matrix Metalloproteinase 9 (EC 3.4.24.35)
Language	English
Publishing date	2023-11-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2041352-X
ISSN	1471-2407 ; 1471-2407
ISSN (online)	1471-2407
ISSN	1471-2407
DOI	10.1186/s12885-023-11612-9
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Article: Qizhu Anti-Cancer Recipe promotes anoikis of hepatocellular carcinoma cells by activating the c-Jun N-terminal kinase pathway.

Han, Zhiyi / Huang, Qi / Lv, Minling / Ma, Mengqing / Zhang, Wei / Feng, Wenxing / Hu, Rui / Sun, Xinfeng / Li, Jing / Zhong, Xin / Zhou, Xiaozhou

Heliyon

2023 Volume 9, Issue 11, Page(s) e22089

Abstract: Background: Qizhu Anti-Cancer Recipe (QACR) is a traditional Chinese medicine widely used in treating several liver diseases. However, its function and the relevant mechanism underlying its effect in treating hepatocellular carcinoma (HCC) remain ... ...

Abstract	Background: Qizhu Anti-Cancer Recipe (QACR) is a traditional Chinese medicine widely used in treating several liver diseases. However, its function and the relevant mechanism underlying its effect in treating hepatocellular carcinoma (HCC) remain unknown. The aim of this study was to explore the effect of QACR in HCC, which are expected to be a potential therapeutic scheme for HCC. Materials and methods: The chemical compositions of QACR were determined by liquid chromatography/quadrupole time-of-fight mass spectrometry (LC-QTOF-MS). The anoikis-resistant HCC cell proliferation and angiopoiesis were detected using the cell counting kit 8 (CCK8) assay, trypan blue, calcein AM/EthD-1, flow cytometer, Western blot, and tube formation assays. An orthotopic xenograft mouse model was established to evaluate the Results: QACR reduced the growth and tube formation of anoikis-resistant HCC cells and enhanced cell apoptosis Conclusion: Our study suggests that QACR suppresses the proliferation and angiopoiesis of anoikis-resistant HCC cells by activating the JNK pathway. Therefore, QACR is a promising new therapeutic strategy for treating hepatocellular carcinoma.
Language	English
Publishing date	2023-11-13
Publishing country	England
Document type	Journal Article
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2023.e22089
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Article ; Online: High shear stress attenuated arterial neointimal hyperplasia accompanied by changes in yes-associated protein/jun N-terminal kinase/vascular cell adhesion protein 1 expression.

Chen, Feng / Luo, Jun Fu / Wan, Rong

Vascular

2022 Volume 31, Issue 1, Page(s) 163–173

Abstract: Background and objectives: Abnormal neointimal hyperplasia (NIH) is known as the predominant mechanism in the pathogenesis of arterial restenosis after balloon angioplasty. Low shear stress (SS) is known to augment balloon injury-induced NIH. The aim of ...

Abstract	Background and objectives: Abnormal neointimal hyperplasia (NIH) is known as the predominant mechanism in the pathogenesis of arterial restenosis after balloon angioplasty. Low shear stress (SS) is known to augment balloon injury-induced NIH. The aim of this study is to study the effect and mechanisms of an increase of shear stress caused by arteriovenous fistula could alleviate arterial NIH caused by balloon injury. Methods and results: Eighteen male rabbits were randomly divided into three groups: BI-the rabbits received a balloon injury to right common carotid artery (CCA). BI+AVF-the rabbits received a balloon injury to right CCA and a carotid-jugular AVF. Control-the animals received no surgery. After 21 days, CCA samples were harvested for histological staining, immunohistochemistry, and western blot analysis. The luminal shear stress of the BI+AVF group increased from 13.8 ± 1.0 dyn/cm Conclusion: The arteriovenous fistula alleviated the balloon injury-induced arterial NIH. It elevated the luminal shear stress and inhibited SMCs phenotypic modulation to the synthetic state, as well as suppressing the over-activation of YAP, JNK, and VCAM1.
MeSH term(s)	Animals ; Male ; Rabbits ; Hyperplasia ; Neointima ; JNK Mitogen-Activated Protein Kinases ; Cell Adhesion ; YAP-Signaling Proteins ; Cell Proliferation ; Arteriovenous Fistula
Chemical Substances	JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; YAP-Signaling Proteins
Language	English
Publishing date	2022-01-17
Publishing country	England
Document type	Journal Article
ZDB-ID	2137151-9
ISSN	1708-539X ; 1708-5381
ISSN (online)	1708-539X
ISSN	1708-5381
DOI	10.1177/17085381211058335
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Zs.A 4277: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: B4GALNT1 promotes progression and metastasis in lung adenocarcinoma through JNK/c-Jun/Slug pathway.

Jiang, Tian / Wu, Hao / Lin, Miao / Yin, Jun / Tan, Lijie / Ruan, Yuanyuan / Feng, Mingxiang

Carcinogenesis

2020 Volume 42, Issue 4, Page(s) 621–630

Abstract: ... the JNK/c-Jun/Slug pathway, and with the form of its enzymatic activity. Clinical samples confirmed ... that B4GALNT1 expression was upregulated in LUAD, and B4GALNT1 was correlated with c-Jun/Slug expression ... suggest that B4GALNT1 promotes progression and metastasis of LUAD through activating JNK/c-Jun/Slug ...

Abstract	Lung adenocarcinoma (LUAD) is one of the most common types of cancer and has a low survival rate. β-1,4-N-Acetyl galactosaminyltransferase 1 (B4GALNT1), which is involved in the synthesis of complex gangliosides, is highly expressed in the progression of various cancers. This study aimed to elucidate the biological functions of B4GALNT1 in LUAD progression and metastasis. We observed that B4GALNT1 overexpression showed enhanced cell migration and invasion in vitro, and promoted tumor metastasis, with reduced survival in mice. Mechanistically, B4GALNT1 regulated metastatic potential of LUAD through activating the JNK/c-Jun/Slug pathway, and with the form of its enzymatic activity. Clinical samples confirmed that B4GALNT1 expression was upregulated in LUAD, and B4GALNT1 was correlated with c-Jun/Slug expression, lymph node involvement, advanced clinical stage, and reduced overall survival. Collectively, our results suggest that B4GALNT1 promotes progression and metastasis of LUAD through activating JNK/c-Jun/Slug signaling, and with the form of its enzymatic activity.
MeSH term(s)	Adenocarcinoma of Lung/genetics ; Adenocarcinoma of Lung/pathology ; Animals ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation/genetics ; Disease Progression ; Female ; Gene Expression Regulation, Neoplastic/genetics ; Heterografts ; Humans ; JNK Mitogen-Activated Protein Kinases/genetics ; MAP Kinase Kinase 4/genetics ; Male ; Mice ; N-Acetylgalactosaminyltransferases/genetics ; Neoplasm Metastasis ; Signal Transduction ; Snail Family Transcription Factors/genetics
Chemical Substances	SNAI1 protein, human ; Snail Family Transcription Factors ; N-Acetylgalactosaminyltransferases (EC 2.4.1.-) ; B4galnt1 protein, human (EC 2.4.1.165) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; MAP Kinase Kinase 4 (EC 2.7.12.2)
Language	English
Publishing date	2020-12-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603134-1
ISSN	1460-2180 ; 0143-3334
ISSN (online)	1460-2180
ISSN	0143-3334
DOI	10.1093/carcin/bgaa141
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Article ; Online: BUB1B promotes extrahepatic cholangiocarcinoma progression via JNK/c-Jun pathways.

Jiao, Chen Yu / Feng, Qin Chao / Li, Chang Xian / Wang, Dong / Han, Sheng / Zhang, Yao Dong / Jiang, Wang Jie / Chang, Jiang / Wang, Xuehao / Li, Xiang Cheng

Cell death & disease

2021 Volume 12, Issue 1, Page(s) 63

Abstract: ... the opposite effect. Furthermore, the activation of c-Jun N-terminal kinase-c-Jun (JNK)-c-Jun pathway was ... regulated by BUB1B. BUB1B regulated the proliferation and invasiveness of CAA cells in a JNK-c-Jun-dependent ... promoted ECC progression via JNK/c-Jun pathways. These findings suggested that BUB1B could be a potential ...

Abstract	Currently, the controversy regarding the expression profile and function of BUB1B in different malignancies still exist. In this project, we aimed to explore the role and molecular mechanism of BUB1B in the progression of extrahepatic cholangiocarcinoma (ECC). The expression levels of BUB1B in human ECC were evaluated by immunohistochemistry, western blot, and real-time PCR. The role and mechanism of BUB1B in CCA cell proliferation and invasion were investigated in both in vitro and in vivo functional studies. To indicate the clinical significance, a tissue microarray was performed on 113 ECC patients, followed by univariate and multivariate analyses. The expression of BUB1B was increased in both human CCA tissues and CCA cells. Results from loss-of-function and gain-of-function experiments suggested that the inhibition of BUB1B decreased the proliferation and invasiveness of CCA cells in vitro and in vivo, while overexpression of BUB1B achieved the opposite effect. Furthermore, the activation of c-Jun N-terminal kinase-c-Jun (JNK)-c-Jun pathway was regulated by BUB1B. BUB1B regulated the proliferation and invasiveness of CAA cells in a JNK-c-Jun-dependent manner. Clinically, ECC patients with BUB1B high expression had worse overall survival and recurrence-free survival than those with BUB1B low expression. Multivariate analysis identified that BUB1B was an independent predictor for postoperative recurrence and overall survival of ECC patients. In conclusion, BUB1B promoted ECC progression via JNK/c-Jun pathways. These findings suggested that BUB1B could be a potential therapeutic target and a biomarker for predicting prognosis for ECC patients.
MeSH term(s)	Bile Duct Neoplasms/genetics ; Cell Cycle Proteins/metabolism ; Cell Line, Tumor ; Cholangiocarcinoma/genetics ; Disease Progression ; Humans ; MAP Kinase Signaling System ; Prognosis ; Protein-Serine-Threonine Kinases/metabolism
Chemical Substances	BUB1B protein, human ; Cell Cycle Proteins ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2021-01-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-020-03234-x
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Article ; Online: C-Jun/C7ORF41/NF-κB axis mediates hepatic inflammation and lipid accumulation in NAFLD.

Yan, Feng-Juan / Wang, Xu / Wang, Song-En / Hong, Hai-Ting / Lu, Jun / Ye, Qin / Zheng, Yuan-Lin / Wang, Yong-Jian

The Biochemical journal

2020 Volume 477, Issue 3, Page(s) 691–708

Abstract: ... activation, which promotes c-Jun-mediated transcriptional repression of C7ORF41. In conclusion, our findings ... suggested that a c-Jun/C7ORF41/NF-κB regulatory network controls the inflammatory response and lipid ...

Abstract	Nonalcoholic fatty liver disease (NAFLD) is an expanding health problem worldwide. Although many studies have made great efforts to elucidate the pathogenesis of NAFLD, the molecular basis remains poorly understood. Here, we showed that hepatic C7ORF41, a critical regulator of innate immune response, was markedly decreased in diet or genetic-induced NAFLD model. We also demonstrated that C7ORF41 overexpression significantly ameliorated hepatic inflammation and lipid accumulation in palmitic acid (PA)-treated hepatocytes, whereas C7ORF41 knockdown showed the opposite effects. Mechanistically, we found the anti-inflammatory role of C7ORF41 was attributed to the suppression of NF-κB p65-mediated induction of inflammatory cytokines. Moreover, we demonstrated that the suppression of C7ORF41 expression in hepatocytes is due to JNK activation, which promotes c-Jun-mediated transcriptional repression of C7ORF41. In conclusion, our findings suggested that a c-Jun/C7ORF41/NF-κB regulatory network controls the inflammatory response and lipid accumulation in NAFLD and may benefit the development of novel and promising therapeutic targets for NAFLD.
MeSH term(s)	Animals ; Cytokines/metabolism ; Disease Models, Animal ; Hepatocytes/pathology ; Immunity, Innate ; Inflammation/metabolism ; JNK Mitogen-Activated Protein Kinases/metabolism ; Lipid Metabolism ; Liver/pathology ; Mice ; NF-kappa B/metabolism ; Non-alcoholic Fatty Liver Disease/metabolism ; Signal Transduction
Chemical Substances	Cytokines ; NF-kappa B ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2020-01-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2969-5
ISSN	1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
ISSN (online)	1470-8728
ISSN	0006-2936 ; 0306-3275 ; 0264-6021
DOI	10.1042/BCJ20190799
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Article ; Online: c-Jun N-terminal kinase activation contributes to improving low temperature tolerance via regulating apoptosis in the Pacific white shrimp Penaeus vannamei.

Zheng, JieRen / Zhao, Ying / Feng, YuXin / Qian, WeiGuo / Zhang, Yu / Dong, BeiBei / Liang, QingJian

Fish & shellfish immunology

2023 Volume 139, Page(s) 108912

Abstract: ... c-Jun N-terminal kinase (JNK) is involved in regulating various physiological processes, including ...

Abstract	Temperature is an essential environmental factor for the survival of aquatic animals. Low temperature stress can induce mitochondria to produce excessive ROS and free radicals, and destroy homeostasis. c-Jun N-terminal kinase (JNK) is involved in regulating various physiological processes, including inflammatory responses, cell cycle, reproduction, and apoptosis. Here, we investigated the mechanism of ROS/JNK pathway under low temperature stress both in vitro and in vivo. In this study, transcriptome analysis revealed that apoptosis, autophagy, calcium channel, and antioxidant were involved in the mediation of low temperature tolerance in Pacific white shrimp (penaeus vannamei). PvJNK was activated in response to low temperature stress. Treatments with different temperature caused oxidative stress as demonstrated by increased intensity of the ROS indicator H
MeSH term(s)	Animals ; JNK Mitogen-Activated Protein Kinases/genetics ; Reactive Oxygen Species/metabolism ; Penaeidae/genetics ; Penaeidae/metabolism ; Temperature ; Apoptosis/genetics
Chemical Substances	JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Reactive Oxygen Species
Language	English
Publishing date	2023-06-21
Publishing country	England
Document type	Journal Article
ZDB-ID	1067738-0
ISSN	1095-9947 ; 1050-4648
ISSN (online)	1095-9947
ISSN	1050-4648
DOI	10.1016/j.fsi.2023.108912
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Article ; Online: c-Jun-mediated miR-19b expression induces endothelial barrier dysfunction in an in vitro model of hemorrhagic shock.

Wu, Feng / Wang, Jian-Ying / Dorman, Brooke / Zeineddin, Ahmad / Kozar, Rosemary Ann

Molecular medicine (Cambridge, Mass.)

2022 Volume 28, Issue 1, Page(s) 123

Abstract: ... if c-Jun mediates the early responsive microRNA, miR-19b, to cause endothelial barrier dysfunction ... Method: Human lung microvascular endothelial cells (HLMEC) or HEK293T cells were transfected with c-Jun ... overexpressing vector, c-Jun siRNA, miR-19b promoter vector, miR-19b mutated promoter vector, miR-19b oligo ...

Abstract	Background: Our previous data demonstrated that miR-19b expression was increased in human lung microvascular endothelial cells in-vitro-, in-vivo and in patients with hemorrhagic shock, leading to a decrease in syndecan-1 mRNA and protein and resulting in loss of endothelial barrier function. However, the mechanism underlying increased miR-19b expression remains unclear. The objective of the current study was to determine if c-Jun mediates the early responsive microRNA, miR-19b, to cause endothelial barrier dysfunction. Method: Human lung microvascular endothelial cells (HLMEC) or HEK293T cells were transfected with c-Jun overexpressing vector, c-Jun siRNA, miR-19b promoter vector, miR-19b mutated promoter vector, miR-19b oligo inhibitor, then subjected to hypoxia/reoxygenation as in-vitro model of hemorrhagic shock. Levels of protein, miRNA, and luciferase activity were measured. Transwell permeability of endothelial monolayers were also determined. Plasma levels of c-Jun were measured in injured patients with hemorrhagic shock. Result: Hypoxia/reoxygenation induced primary (pri-)miR-19b, mature miR-19b, and c-Jun expression over time in a comparable timeframe. c-Jun silencing by transfection with its specific siRNA reduced both pri-miR-19b and mature miR-19b levels. Conversely, c-Jun overexpression enhanced H/R-induced pri-miR-19b. Studies using a luciferase reporter assay revealed that in cells transfected with vectors containing the wild-type miR-19b promoter and luciferase reporter, c-Jun overexpression or hypoxia/ reoxygenation significantly increased luciferase activity. c-Jun knockdown reduced the luciferase activity in these cells, suggesting that the miR-19b promoter is directly activated by c-Jun. Further, chromatin immunoprecipitation assay confirmed that c-Jun directly bound to the promoter DNA of miR-19b and hypoxia/reoxygenation significantly increased this interaction. Additionally, c-Jun silencing prevented cell surface syndecan-1 loss and endothelial barrier dysfunction in HLMECs after hypoxia/reoxygenation. Lastly, c-Jun was significantly elevated in patients with hemorrhagic shock compared to healthy controls. Conclusion: Transcription factor c-Jun is inducible by hypoxia/reoxygenation, binds to and activates the miR-19b promoter. Using an in-vitro model of hemorrhagic shock, our findings identified a novel cellular mechanism whereby hypoxia/ reoxygenation increases miR-19b transcription by inducing c-Jun and leads to syndecan-1 decrease and endothelial cell barrier dysfunction. This finding supports that miR-19b could be a potential therapeutic target for hemorrhage shock.
MeSH term(s)	Endothelial Cells/metabolism ; HEK293 Cells ; Humans ; Hypoxia/metabolism ; MicroRNAs/metabolism ; Proto-Oncogene Proteins c-jun/metabolism ; RNA, Messenger/metabolism ; RNA, Small Interfering ; Shock, Hemorrhagic/genetics ; Shock, Hemorrhagic/metabolism ; Syndecan-1/metabolism ; Transcription Factors/metabolism
Chemical Substances	MicroRNAs ; Proto-Oncogene Proteins c-jun ; RNA, Messenger ; RNA, Small Interfering ; Syndecan-1 ; Transcription Factors
Language	English
Publishing date	2022-10-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1283676-x
ISSN	1528-3658 ; 1076-1551
ISSN (online)	1528-3658
ISSN	1076-1551
DOI	10.1186/s10020-022-00550-0
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