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Article ; Online: SENP3-mediated deSUMOylation of c-Jun facilitates microglia-induced neuroinflammation after cerebral ischemia and reperfusion injury.

Xia, Qian / Mao, Meng / Zhan, Gaofeng / Luo, Zhenzhao / Zhao, Yin / Li, Xing

iScience

2023 Volume 26, Issue 6, Page(s) 106953

Abstract: Recent evidences have implicated that SENP3 is a deSUMOylase which possesses neuronal damage effects in cerebral ischemia. However, its role in microglia remains poorly understood. Here, we found that SENP3 was upregulated in the peri-infarct areas of ... ...

Abstract	Recent evidences have implicated that SENP3 is a deSUMOylase which possesses neuronal damage effects in cerebral ischemia. However, its role in microglia remains poorly understood. Here, we found that SENP3 was upregulated in the peri-infarct areas of mice following ischemic stroke. Furthermore, knockdown of SENP3 significantly inhibits the expression of proinflammatory cytokines and chemokines in microglial cells. Mechanistically, SENP3 can bind and then mediated the deSUMOylation of c-Jun, which activated its transcriptional activity, ultimately followed by the activation of MAPK/AP-1 signaling pathway. In addition, microglia-specific SENP3 knockdown alleviated ischemia-induced neuronal damage, and markedly diminished infract volume, ameliorated sensorimotor and cognitive function in animals subjected to ischemic stroke. These results indicated SENP3 functions as a novel regulator of microglia-induced neuroinflammation by activating the MAPK/AP-1 signaling pathway via mediating the deSUMOylation of c-Jun. Interventions of SENP3 expression or its interaction with c-Jun would be a new and promising therapeutic strategy for ischemic stroke.
Language	English
Publishing date	2023-05-25
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.106953
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Article ; Online: Tat-NTS Suppresses the Proliferation, Migration and Invasion of Glioblastoma Cells by Inhibiting Annexin-A1 Nuclear Translocation.

Luo, Zhenzhao / Liu, Li / Li, Xing / Chen, Weiqun / Lu, Zhongxin

Cellular and molecular neurobiology

2021 Volume 42, Issue 8, Page(s) 2715–2725

Abstract: Prevention of the nuclear translocation of ANXA1 with Tat-NTS was recently reported to alleviate neuronal injury and protect against cerebral stroke. However, the role that Tat-NTS plays in the occurrence and development of gliomas still needs to be ... ...

Abstract	Prevention of the nuclear translocation of ANXA1 with Tat-NTS was recently reported to alleviate neuronal injury and protect against cerebral stroke. However, the role that Tat-NTS plays in the occurrence and development of gliomas still needs to be elucidated. Therefore, human glioblastoma (GB) cells were treated with various concentrations of Tat-NTS for 24 h, and cell proliferation, migration and invasion were assessed with CCK-8 and Transwell assays. The nuclear translocation of ANXA1 was evaluated by subcellular extraction and immunofluorescence, and protein expression levels were detected by Western blot analysis. In addition, the activity of MMP-2/9 was measured by gelatin zymography. The results revealed that Tat-NTS significantly inhibited the nuclear translocation of ANXA1 in U87 cells and inhibited the proliferation, migration and invasion of GB cells. Tat-NTS also suppressed cell cycle regulatory proteins and MMP-2/-9 activity and expression. Moreover, Tat-NTS reduced the level of p-p65 NF-κB in U87 cells. These results suggest that the Tat-NTS-induced inhibition of GB cell proliferation, migration and invasion is closely associated with the induction of cell cycle arrest, downregulation of MMP-2/-9 expression and activity and suppression of the NF-κB signaling pathway. Thus, Tat-NTS may be a potential chemotherapeutic agent for the treatment of GB.
MeSH term(s)	Annexin A1/metabolism ; Cell Cycle Proteins/metabolism ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Gelatin ; Glioblastoma/drug therapy ; Glioblastoma/metabolism ; Humans ; Matrix Metalloproteinase 2/metabolism ; NF-kappa B/metabolism ; Neoplasm Invasiveness ; Sincalide/metabolism
Chemical Substances	Annexin A1 ; Cell Cycle Proteins ; NF-kappa B ; Gelatin (9000-70-8) ; Matrix Metalloproteinase 2 (EC 3.4.24.24) ; Sincalide (M03GIQ7Z6P)
Language	English
Publishing date	2021-08-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	283404-2
ISSN	1573-6830 ; 0272-4340
ISSN (online)	1573-6830
ISSN	0272-4340
DOI	10.1007/s10571-021-01134-y
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Article ; Online: Correction to: Tat-NTS Suppresses the Proliferation, Migration and Invasion of Glioblastoma Cells by Inhibiting Annexin-A1 Nuclear Translocation.

Luo, Zhenzhao / Liu, Li / Li, Xing / Chen, Weiqun / Lu, Zhongxin

Cellular and molecular neurobiology

2021 Volume 42, Issue 8, Page(s) 2727–2732

Language	English
Publishing date	2021-09-03
Publishing country	United States
Document type	Published Erratum
ZDB-ID	283404-2
ISSN	1573-6830 ; 0272-4340
ISSN (online)	1573-6830
ISSN	0272-4340
DOI	10.1007/s10571-021-01143-x
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Article ; Online: Inhibition of SENP6 restrains cerebral ischemia-reperfusion injury by regulating Annexin-A1 nuclear translocation-associated neuronal apoptosis.

Xia, Qian / Mao, Meng / Zeng, Zhen / Luo, Zhenzhao / Zhao, Yin / Shi, Jing / Li, Xing

Theranostics

2021 Volume 11, Issue 15, Page(s) 7450–7470

Abstract: Rationale: ...

Abstract	Rationale:
MeSH term(s)	Active Transport, Cell Nucleus ; Animals ; Annexin A1/metabolism ; Apoptosis ; Cell Nucleus/metabolism ; Cell Nucleus/pathology ; Cysteine Endopeptidases/metabolism ; Ischemic Stroke/metabolism ; Ischemic Stroke/pathology ; Mice ; Neurons/metabolism ; Neurons/pathology ; Reperfusion Injury/metabolism ; Reperfusion Injury/pathology
Chemical Substances	Annexin A1 ; annexin A1, mouse ; Cysteine Endopeptidases (EC 3.4.22.-) ; Senp6 protein, mouse (EC 3.4.22.-)
Language	English
Publishing date	2021-06-01
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592097-2
ISSN	1838-7640 ; 1838-7640
ISSN (online)	1838-7640
ISSN	1838-7640
DOI	10.7150/thno.60277
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Article ; Online: Knockdown of Annexin-A1 Inhibits Growth, Migration and Invasion of Glioma Cells by Suppressing the PI3K/Akt Signaling Pathway.

Wei, Liqing / Li, Li / Liu, Li / Yu, Ru / Li, Xing / Luo, Zhenzhao

ASN neuro

2021 Volume 13, Page(s) 17590914211001218

Abstract: ANXA1, which can bind phospholipid in a calcium dependent manner, is reported to play a pivotal role in tumor progression. However, the role and mechanism of ANXA1 involved in the occurrence and development of malignant glioma are still not well studied. ...

Abstract	ANXA1, which can bind phospholipid in a calcium dependent manner, is reported to play a pivotal role in tumor progression. However, the role and mechanism of ANXA1 involved in the occurrence and development of malignant glioma are still not well studied. Therefore, we explored the effects of ANXA1 on normal astrocytes and glioma cell proliferation, apoptosis, migration and invasion and the underlying mechanisms. We found that ANXA1 was markedly up-regulated in glioma cell lines and glioma tissues. Down-regulation of ANXA1 inhibited normal astrocytes and glioma cell proliferation and induced the cell apoptosis, which suggested that the consequences of loss of Annexin 1 are not specific to the tumor cells. Furthermore, the siRNA-ANXA1 treatment significantly reduced tumor growth rate and tumor weight. Moreover, decreasing ANXA1 expression caused G2/M phase arrest by repressing expression levels of cdc25C, cdc2 and cyclin B1. Interestingly, ANXA1 did not affect the expressions of β-catenin, GSK-3β and NF-κB, the key signaling molecules associated with cancer progression. However, siRNA-ANXA1 was found to negatively regulate phosphorylation of AKT and the expression and activity of MMP2/-9. Finally, the decrease of cell proliferation and invasiveness induced by ANXA1 down-regulation was partially reversed by combined treatment with AKT agonist insulin-like growth factor-1 (IGF-1). Meanwhile, the inhibition of glioma cell proliferation and invasiveness induced by ANXA1 down-regulation was further enhanced by combined treatment with AKT inhibitor LY294002. In summary, these findings demonstrate that ANXA1 regulates proliferation, migration and invasion of glioma cells via PI3K/AKT signaling pathway.
MeSH term(s)	Annexin A1/genetics ; Apoptosis ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Glioma ; Glycogen Synthase Kinase 3 beta ; Humans ; Neoplasm Invasiveness ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction
Chemical Substances	ANXA1 protein, human ; Annexin A1 ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2021-03-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2485467-0
ISSN	1759-0914 ; 1759-0914
ISSN (online)	1759-0914
ISSN	1759-0914
DOI	10.1177/17590914211001218
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Article ; Online: MiR-188-3p and miR-133b Suppress Cell Proliferation in Human Hepatocellular Carcinoma via Post-Transcriptional Suppression of NDRG1.

Luo, Zhenzhao / Fan, Yue / Liu, Xianchang / Liu, Shuiyi / Kong, Xiaoyu / Ding, Zhonghuan / Li, Ying / Wei, Liqing

Technology in cancer research & treatment

2021 Volume 20, Page(s) 15330338211033074

Abstract: Background: Previous studies reported that N-myc downstream-regulated gene 1 (NDRG1) was upregulated in various cancer tissues and decreased expression of miR-188-3p and miR-133b could suppress cell proliferation, metastasis, and invasion and induce ... ...

Abstract	Background: Previous studies reported that N-myc downstream-regulated gene 1 (NDRG1) was upregulated in various cancer tissues and decreased expression of miR-188-3p and miR-133b could suppress cell proliferation, metastasis, and invasion and induce apoptosis of cancer cells. However, the molecular mechanism of NRDG1 involved in hepatocellular carcinoma (HCC) tumorigenesis is still unknown. Methods: The expressions of miR-188-3p, miR-133b, and NRDG1 in HCC tissues and cells were quantified by qRT-PCR and Western blot. MTT assay and transwell invasion assay were performed to evaluate cell growth and cell migration, respectively. Luciferase reporter assay were performed to determine whether miR-188-3p and miR-133b could directly bind to NRDG1 in HCC cells. Results: The results showed that NRDG1 was upregulated and these 2 microRNAs were downregulated in HCC tissues. NRDG1 was negatively correlated with miR-188-3p and miR-133b in HCC tissues. MiR-188-3p and miR-133b were demonstrated to directly bind to 3'UTR of NRDG1 and inhibit its expression. Upregulation of miR-188-3p and miR-133b reduced NRDG1 expression in hepatocellular carcinoma cell lines, which consequently inhibited cell growth and cell migration. Conclusions: Our finding suggested that miR-188-3p and miR-133b exert a suppressive effect on hepatocellular carcinoma proliferation, invasion, and migration through downregulation of NDRG1.
MeSH term(s)	Adult ; Aged ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Movement ; Cell Proliferation ; Down-Regulation ; Female ; Gene Expression Regulation, Neoplastic ; Hep G2 Cells ; Humans ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Male ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Middle Aged ; Transfection
Chemical Substances	Cell Cycle Proteins ; Intracellular Signaling Peptides and Proteins ; MIRN133 microRNA, human ; MIRN188 microRNA, human ; MicroRNAs ; N-myc downstream-regulated gene 1 protein
Language	English
Publishing date	2021-08-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2146365-7
ISSN	1533-0338 ; 1533-0346
ISSN (online)	1533-0338
ISSN	1533-0346
DOI	10.1177/15330338211033074
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Article ; Online: miR-4454 up-regulated by HPV16 E6/E7 promotes invasion and migration by targeting ABHD2/NUDT21 in cervical cancer.

Wang, Hui / Hu, Hui / Luo, Zhenzhao / Liu, Shuiyi / Wu, Wangze / Zhu, Man / Wang, Jing / Liu, Yingle / Lu, Zhongxin

Bioscience reports

2020 Volume 40, Issue 9

Abstract: The abnormal expression of HPV16 E6/E7 activates oncogenes and/or inactivates tumor suppressor genes, resulting in the selective growth and malignant transformation of cancer cells. miR-4454 was selected by sequencing due to its abnormal high expression ... ...

Abstract	The abnormal expression of HPV16 E6/E7 activates oncogenes and/or inactivates tumor suppressor genes, resulting in the selective growth and malignant transformation of cancer cells. miR-4454 was selected by sequencing due to its abnormal high expression in HPV16 E6/E7 positive CaSki cell compared with HPV16 E6/E7 negative C33A cell. Overexpression of miR-4454 enhances cervical cancer cell invasion and migration. ABHD2 and NUDT21 are identified as a target gene of miR-4454.The effects of ABHD2 and NUDT21 on migration and invasion of CaSki and C33A cells were determined. The dual luciferase and RT-qPCR assays confirmed that miR-4454 might regulate its targets ABHD2 and NUDT21 to promote the proliferation, invasion and migration, whereas, inhibit the apoptosis in CaSki and C33A cells.
MeSH term(s)	Apoptosis/genetics ; Cell Line, Tumor ; Cell Movement/genetics ; Cell Proliferation/genetics ; Cleavage And Polyadenylation Specificity Factor/genetics ; Cleavage And Polyadenylation Specificity Factor/metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Hydrolases/genetics ; Hydrolases/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Oncogene Proteins, Viral/genetics ; Oncogene Proteins, Viral/metabolism ; Papillomavirus E7 Proteins/genetics ; Papillomavirus E7 Proteins/metabolism ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Up-Regulation ; Uterine Cervical Neoplasms/genetics ; Uterine Cervical Neoplasms/pathology ; Uterine Cervical Neoplasms/virology
Chemical Substances	Cleavage And Polyadenylation Specificity Factor ; E6 protein, Human papillomavirus type 16 ; MIRN4454 microRNA, human ; MicroRNAs ; Nudt21 protein, human ; Oncogene Proteins, Viral ; Papillomavirus E7 Proteins ; Repressor Proteins ; oncogene protein E7, Human papillomavirus type 16 ; Hydrolases (EC 3.-) ; ABHD2 protein, human (EC 3.1.1.-)
Language	English
Publishing date	2020-08-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	764946-0
ISSN	1573-4935 ; 0144-8463
ISSN (online)	1573-4935
ISSN	0144-8463
DOI	10.1042/BSR20200796
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Article ; Online: Carnitine palmitoyl transferase 1A is a novel diagnostic and predictive biomarker for breast cancer.

Tan, Zheqiong / Zou, Yaru / Zhu, Man / Luo, Zhenzhao / Wu, Tangwei / Zheng, Chao / Xie, Aqing / Wang, Hui / Fang, Shiqiang / Liu, Shuiyi / Li, Yong / Lu, Zhongxin

BMC cancer

2021 Volume 21, Issue 1, Page(s) 409

Abstract: Background: Carnitine palmitoyl transferase 1A (CPT1A), the key regulator of fatty acid oxidation, contributes to tumor metastasis and therapeutic resistance. We aimed to identify its clinical significance as a biomarker for the diagnosis and prediction ...

Abstract	Background: Carnitine palmitoyl transferase 1A (CPT1A), the key regulator of fatty acid oxidation, contributes to tumor metastasis and therapeutic resistance. We aimed to identify its clinical significance as a biomarker for the diagnosis and prediction of breast cancer. Methods: Western blot, ELISA and in silico analysis were used to confirm CPT1A levels in breast cancer cell lines, cell culture medium and breast cancer tissues. Four hundred thirty breast cancer patients, 200 patients with benign breast disease, and 400 healthy controls were enrolled and randomly divided into a training set and a test set with a 7:3 ratio. Training set was used to build diagnostic models and 10-fold cross validation was used to demonstrate the performance of the models. Then test set was aimed to validate the effectiveness of the diagnostic models. ELISA was conducted to detect individual serum CPT1A levels. Receiver operating characteristic (ROC) curves were generated, and binary logistic regression analyses were performed to evaluate the effectiveness of CPT1A as a biomarker in breast cancer diagnosis. CPT1A levels between post-operative and pre-operative samples were also compared. Results: CPT1A was overexpressed in breast cancer tissues, cell lines and cell culture medium. Serum CPT1A levels were higher in breast cancer patients than in controls and were significantly associated with metastasis, TNM stage, histological grading and molecular subtype. CPT1A levels were decreased in post-operative samples compared with paired pre-operative samples. Moreover, CPT1A exhibited a higher efficacy in differentiating breast cancer patients from healthy controls (training set: area under the curve, AUC, 0.892, 95% CI, 0.872-0.920; test set, AUC, 0.904, 95% CI, 0.869-0.939) than did CA15-3, CEA, or CA125. Conclusion: CPT1A is overexpressed in breast cancer and can be secreted out of breast cancer cell. Serum CPT1A is positively associated with breast cancer progression and could serve as an indicator for disease monitoring. Serum CPT1A displayed a remarkably high diagnostic efficiency for breast cancer and could be a novel biomarker for the diagnosis of breast cancer.
MeSH term(s)	Adult ; Aged ; Biomarkers, Tumor ; Breast Diseases/diagnosis ; Breast Diseases/enzymology ; Breast Neoplasms/diagnosis ; Breast Neoplasms/enzymology ; Breast Neoplasms/mortality ; Carnitine O-Palmitoyltransferase/blood ; Carnitine O-Palmitoyltransferase/metabolism ; Case-Control Studies ; Cell Line, Tumor ; Enzyme-Linked Immunosorbent Assay ; Female ; Humans ; Middle Aged ; Neoplasm Metastasis ; Neoplasm Staging ; Prognosis ; ROC Curve ; Reproducibility of Results
Chemical Substances	Biomarkers, Tumor ; CPT1A protein, human (EC 2.3.1.21) ; Carnitine O-Palmitoyltransferase (EC 2.3.1.21)
Language	English
Publishing date	2021-04-15
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/s12885-021-08134-7
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Article ; Online: Association of the vitamin D metabolism gene GC and CYP27B1 polymorphisms with cancer susceptibility: a meta-analysis and trial sequential analysis.

Zhu, Man / Tan, Zheqiong / Luo, Zhenzhao / Hu, Hui / Wu, Tangwei / Fang, Shiqiang / Wang, Hui / Lu, Zhongxin

Bioscience reports

2019 Volume 39, Issue 9

Abstract: Nowadays, vitamin D is known to have functions beyond bone formation, including inhibiting angiogenesis and promoting tumor apoptosis. CYP27B1 and group-specific component (GC), the main enzyme responsible for the degradation and transport of active ... ...

Abstract	Nowadays, vitamin D is known to have functions beyond bone formation, including inhibiting angiogenesis and promoting tumor apoptosis. CYP27B1 and group-specific component (GC), the main enzyme responsible for the degradation and transport of active vitamin D, play important role in many cancer-related cellular processes. Relationships between CYP27B1 and GC polymorphisms and cancer susceptibility have been widely investigated, whereas the results are inconsistent. We strictly searched EMBASE, PubMed, Web of Science, WanFang and CNKI electronic databases for relevant studies exploring the associations of GC (rs4588 and rs7041) and CYP27B1 (rs4646537, rs3782130) polymorphisms with cancer risks according to search strategy. Thirty-two studies published in 13 articles involving 15713 cases and 17304 controls were included. Our analyses suggested that rs4588 and rs7041 polymorphisms were significantly associated with overall cancer risk. Stratification analyses of ethnicity indicated that rs4588 polymorphism significantly increased cancer risk in Caucasians and Asians, while rs7041 polymorphism significantly increased cancer risk in Asians. When studies were stratified by cancer type, our results indicated that rs4588 significantly increased the risk of breast cancer and digestive system tumor, but not in prostate cancer and non-small cell lung cancer, while rs7041 significantly increased the risk of non-small cell lung cancer. Above associations were noteworthy findings as evaluated by false-positive report probabilities (FPRPs). There were no associations of rs4646537 and rs3782130 with overall cancer risks. Associations between CYP27B1 and GC polymorphisms and cancer risks were examined, and additional large samples are necessary to validate our results.
MeSH term(s)	25-Hydroxyvitamin D3 1-alpha-Hydroxylase/genetics ; Female ; Gene Frequency/genetics ; Genetic Predisposition to Disease/genetics ; Humans ; Male ; Neoplasms/genetics ; Neoplasms/pathology ; Polymorphism, Single Nucleotide/genetics ; Risk ; Vitamin D/metabolism ; Vitamin D-Binding Protein/genetics
Chemical Substances	GC protein, human ; Vitamin D-Binding Protein ; Vitamin D (1406-16-2) ; 25-Hydroxyvitamin D3 1-alpha-Hydroxylase (EC 1.14.15.18) ; CYP27B1 protein, human (EC 1.14.15.18)
Language	English
Publishing date	2019-09-13
Publishing country	England
Document type	Journal Article ; Meta-Analysis ; Research Support, Non-U.S. Gov't
ZDB-ID	764946-0
ISSN	1573-4935 ; 0144-8463
ISSN (online)	1573-4935
ISSN	0144-8463
DOI	10.1042/BSR20190368
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Article ; Online: Annexin-1 Mimetic Peptide Ac2-26 Suppresses Inflammatory Mediators in LPS-Induced Astrocytes and Ameliorates Pain Hypersensitivity in a Rat Model of Inflammatory Pain.

Luo, Zhenzhao / Wang, Hui / Fang, Shiqiang / Li, Li / Li, Xing / Shi, Jing / Zhu, Man / Tan, Zheqiong / Lu, Zhongxin

Cellular and molecular neurobiology

2019 Volume 40, Issue 4, Page(s) 569–585

Abstract: Ac2-26, a mimetic peptide of Annexin-A1, plays a vital role in the anti-inflammatory response mediated by astrocytes. In this study, we aimed to explore the underlying mechanisms of Ac2-26-mediated anti-inflammatory effect. Specifically, we investigated ... ...

Abstract	Ac2-26, a mimetic peptide of Annexin-A1, plays a vital role in the anti-inflammatory response mediated by astrocytes. In this study, we aimed to explore the underlying mechanisms of Ac2-26-mediated anti-inflammatory effect. Specifically, we investigated the inhibitory effects of Ac2-26 on lipopolysaccharide (LPS)-induced astrocyte migration and on pro-inflammatory cytokines and chemokines expressions, as well as one glutathione (GSH) reductase mRNA and total intracellular GSH levels in LPS-induced astrocytes. Additionally, we investigated whether mitogen-activated protein kinases (MAPK) and nuclear factor kappa-B (NF-κB) signaling pathway were involved in this process. Finally, we evaluated the analgesic effect of Ac2-26 in complete Freund's adjuvant (CFA)-induced inflammatory pain model. Our results demonstrated that Ac2-26 inhibited LPS-induced astrocytes migration, reduced the production of pro-inflammatory mediators [tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1 (MIP-1α)] and upregulated GSH reductase mRNA and GSH levels in LPS-induced astrocytes in vitro. This process was mediated through the p38, JNK-MAPK signaling pathway, but not dependent on the NF-κB pathway. Furthermore, the p38 and JNK inhibitors mimicked the effects of Ac2-26, whereas a p38 and JNK activator anisomycin partially reversed its function. Finally, Ac2-26 treatment reduced CFA-induced activation of astrocytes and production of inflammatory mediators in the spinal cord. These results suggest that Ac2-26 attenuates pain by inhibiting astrocyte activation and the production of inflammatory mediators; thus, this work presents Ac2-26 as a potential drug to treat neuropathic pain.
MeSH term(s)	Amino Acid Sequence ; Animals ; Annexins/chemistry ; Astrocytes/metabolism ; Astrocytes/pathology ; Disease Models, Animal ; Hyperalgesia/complications ; Hyperalgesia/drug therapy ; Inflammation/complications ; Inflammation/drug therapy ; Inflammation Mediators/metabolism ; Lipopolysaccharides ; Male ; Pain/complications ; Pain/drug therapy ; Peptides/chemistry ; Peptides/pharmacology ; Peptides/therapeutic use ; Rats, Sprague-Dawley
Chemical Substances	Annexins ; Inflammation Mediators ; Lipopolysaccharides ; Peptides
Language	English
Publishing date	2019-11-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	283404-2
ISSN	1573-6830 ; 0272-4340
ISSN (online)	1573-6830
ISSN	0272-4340
DOI	10.1007/s10571-019-00755-8
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