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Lysophosphatidic acid induced nuclear translocation of nuclear factor-κB in Panc-1 cells by mobilizing cytosolic free calcium

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World Journal of Gastroenterology 2008年第28期14卷 4473-4479页

作者： Yoshiyuki Arita Tetsuhide Ito Takamasa Oono Ken Kawabe Terumasa Hisano Ryoichi Takayanagi Department of Medicine and Bioregulatory Science Graduate School of Medical SciencesKyushu UniversityFukuoka 812-8582Japan

AIM: To clarify whether Lysophosphatidic acid (LPA) activates the nuclear translocation of nuclear factor-κB (NF-κB) in pancreatic cancer. METHODS: Panc-1, a human pancreatic cancer cell line, was used throughout the study. The expression of LPA receptors was confirmed by reverse-transcript polymerase chain reaction (RT-PCR). Cytosolic free calcium was measured by fluorescent calcium indicator fura-2, and the localization of NF-κB was visualized by immunofluorescent method with or without various agents, which effect cell signaling. RESULTS: Panc-1 expressed LPA receptors, LPA1, LPA2 and LPA3. LPA caused the elevation of cytosolic free calcium dose-dependently. LPA also caused the nuclear translocation of NF-κB. Cytosolic free calcium was attenuated by pertussis toxin (PTX) and U73122, an inhibitor of phospholipase C. The translocation of NF-κB was similarly attenuated by PTX and U73122, but phorbol ester, an activator of protein kinase C, alone did not translocate NF-κB. Furthermore, the translocation of NF-κB was completely blocked by Ca2+ chelator BAPTA-AM. Thapsigargin, an endoplasmic- reticulum Ca2+-ATPase pump inhibitor, also promoted the translocation of NF-κB. Staurosporine, a proteinkinase C inhibitor, attenuated translocation of NF-κB induced by LPA. CONCLUSION: These findings suggest that protein kinase C is activated endogenously in Panc-1, and protein kinase C is essential for activating NF-κB with cytosolic calcium and that LPA induces the nuclear translocation of NF-κB in Panc-1 by mobilizing cytosolic free calcium.

关键词： Lysophosphatidic acid nuclear translocation nuclear factor-κB Cytosolic free calcium Panc-1

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Studies on Differential nuclear translocation Mechanism and Assembly of the Three Subunits of the Arabidopsis thaliana Transcription Factor NF-Y

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Molecular Plant 2012年第4期5卷 876-888页

作者： Dieter Hackenberg Yanfang Wu Andrea Voigt Robert Adams Peter Schramm Bernhard GrimmI Institute of Biology/Plant Physiology Humboldt University Philippstr. 13 Building 12 10115 Berlin Germany

The eukaryotic transcription factor NF-Y consists of three subunits （A, B, and C）, which are encoded in Ara- bidopsis thaliana in multigene families consisting of 10, 13, and 13 genes, respectively. In principle, all potential combi- nations of the subunits are possible for the assembly of the heterotrimeric complex. We aimed at assessing the probability of each subunit to participate in the assembly of NF-Y. The evaluation of physical interactions among all members of the NF-Y subunit families indicate a strong requirement for NF-YB/NF-YC heterodimerization before the entire complex can be accomplished. By means of a modified yeast two-hybrid system assembly of all three subunits to a heterotrimeric complex was demonstrated. Using GFP fusion constructs, NF-YA and NF-YC localization in the nucleus was demonstrated, while NF- YB is solely imported into the nucleus as a NF-YC-associated heterodimer NF-YC. This piggyback transport of the two Arabidopsis subunits differs from the import of the NF-Y heterotrimer of heterotrophic organisms. Based on a peptide structure model of the histone-fold-motifs, disulfide bonding among intramolecular conserved cysteine residues of NF-YB, which is responsible for the redox-regulated assembly of NF-YB and NF-YC in human and Aspergillus nidulans, can be excluded for Arabidopsis NF-YB.

关键词： gene expression transcriptional control and transcription factors nuclear translocation protein-proteininteraction.

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Hepatitis C Virus non-structural 5A abrogates signal transducer and activator of transcription-1 nuclear translocation induced by IFN-α through dephosphorylation

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World Journal of Gastroenterology 2007年第30期13卷 4080-4084页

作者： Guo-Zhong Gong Jie Cao Yong-Fang Jiang Yang Zhou Bo Liu Institute of Hepatology and Department of Infectious Diseases The Second Xiangya Hospital Central South University Changsha 410011 Hunan Province China

AIM： To study the effect of Hepatitis C virus nonstructural 5A （HCV NSSA） on IFNα induced signal transducer and activator of transcription-1 （STAT1） phosphorylation and nuclear translocation.METHODS： Expression of STAT1 Tyr701 phosphorylation at different time points was confirmed by Western blot, and the time point when p-STAT1 expressed most, was taken as the IFN induction time for further studies. Immunocytochemistry was used to confirm the successful transient transfection of NS5A expression plasmid. Immunofluorescene was performed to observe if there was any difference in IFNα-induced STAT1 phosphorylation and nuclear translocation between HCV NSSA-expressed and non-HCV NSSA-expressed cells. Western blot was used to compare the phosphorylated STAT1 protein of the cells.RESULTS： Expression of HCV NS5A was found in the cytoplasm of pCNS5A-transfected Huh7 cells, but not in the PRC/ CMV transfected or non-transfected cells, STAT1 Tyr701 phosphorylation was found strongest in 30 min of IFN induction, STAT1 phosphorylation and nuclear import were much less in the presence of HCV NS5A protein in contrast to pRC/CMV-transfected and non-transfected cells under fluorescent microscopy, which was further confirmed by Western blot.CONCLUSION： HCV NSSA expression plasmid is successfully transfected into Huh7 cells and HCV NS5A protein is expressed in the cytoplasm of the cells. IFN-α is able to induce STAT1 phosphrylation and nuclear translocation, and this effect is inhibited by HCV NS5A protein, which might be another possible resistance mechanism to interferon alpha therapy.

关键词： Hepatitis C virus nonstructural protein 5A IFN-α Signal transducer and activator of transcription (STAT1) Phosphorylation nuclear translocation

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CacyBP/SIP nuclear translocation induced by gastrin promotes gastric cancer cell proliferation

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World Journal of Gastroenterology 2014年第29期20卷 10062-10070页

作者： Hui-Hong Zhai Juan Meng Jing-Bo Wang Zhen-Xiong Liu Yuan-Fei Li Shan-Shan Feng Department of Digestive Diseases General Hospital of Ningxia Medical University State Key Laboratory of Cancer Biology Institute of Digestive DiseasesXijing HospitalFourth Military Medical University Surgery Laboratory General Hospital of Ningxia Medical University

AIM: To investigate the role of nuclear translocation of calcyclin binding protein, also called Siah-1 interacting protein (CacyBP/SIP), in gastric carcinogenesis.

关键词： Calcyclin binding protein/Siah-1 interacting protein Gastric caner cells nuclear translocation Gastrin

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Effects of nuclear translocation of tissue transglutaminase and the release of cytochrome C on hepatocyte apoptosis

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Chinese Medical Journal 2003年第5期116卷 742-746页

作者：宋良文马宪梅李扬崔雪梅王晓民 Laboratory of Pathology Beijing Institute of Radiation Medicine Research Beijing 100850 China

Objective To assess the effects of nuclear translocation of tissue transglutaminase (TTG) and the release of cytochrome C on hepatocyte apoptosis and to reveal the mechanism of signal transduction of early apoptosis in injured hepatocytes. Methods Hepatocytes isolated from tissue transglutaminase gene knock-out mice and rats were stimulated with ethanol. Proteins from whole cell, cytoplasm and nuclei were extracted for determination of TTG activity by 14C-putrescine incorporation. Distribution of TTG throughout the entire cell, as well as just nucleus was observed under a confocal scanning microscope. The amount of cytochrome C released from mitochondria was determined by ELISA. Cell apoptosis was observed by fluorescent *** TTG activity in whole cells and nuclei was significantly increased after the hepatocytes were treated with ethanol. Cytochrome C release was remarkably increased in the cells isolated from rat and wild-type mouse after treatment with ethanol but not in TTG gene knock-out mice. Cellular apoptosis appeared in hepatocytes isolated from rats and wild-type mice but not in the hepatocytes from TTG gene knock-out mice after stimulation with *** Increased TTG in hepatocytes can be translocated into the nucleus and promote release of mitochondrial cytochrome C into the cytoplasm. Passing through a series of signal pathways, hepatocyte apoptosis is induced eventually.

关键词： tissue transglutaminase · nuclear translocation · cytochrome C · apoptosis · hepatocyte

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Sulforaphane ameliorates non-alcoholic steatohepatitis by KLF4-mediated macrophage M2 polarization

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Food Science and Human Wellness 2024年第5期13卷 2727-2740页

作者： Xianghui Huang Jia Xu Ye Xu Bingxin Huangfu Feng Zhang Yanzhou Hu Ruxin Gao Xinxin Ren Boyang Zhang Kunlun Huang Xiaoyun He Key Laboratory of Precision Nutrition and Food Quality Key Laboratory of Functional DairyMinistry of EducationCollege of Food Science and Nutritional EngineeringChina Agricultural UniversityBeijing 100083China Key Laboratory of Safety Assessment of Genetically Modified Organism(Food Safety) the Ministry of Agriculture and Rural Affairs of the P.R.ChinaBeijing 100083China

Non-alcoholic fatty liver disease (NAFLD) has become a global issue and a severe threat to public ***, to date, no approved therapeutic drugs have been developed. Dietary interventions with naturalproducts have shown promise in preventing and treating NAFLD. Sulforaphane (SFN) is a phytocompoundwith antioxidant and anti-inflammatory properties, and previous research has demonstrated that SFN canameliorate hepatic lipid accumulation and inflammation. However, the molecular mechanisms underlying thesebeneficial effects remain unclear. In this study, we confirmed the protective effects of SFN on excessive lipidaccumulation and inflammatory injury in a high-fat, high-fructose diet-induced non-alcoholic steatohepatitis(NASH) mouse model. We found that SFN attenuates the inflammatory injury in a macrophage cell line andthe liver of NASH mice, owing to the promotion of M1-type macrophage polarization toward the M2-type andthe regulation of inflammatory mediators. Further analysis demonstrated that this SFN-induced macrophageM2-type polarization occurs in a Krüppel-like factor 4 (KLF4)-dependent manner. In summary, we uncovereda new mechanism of action underlying SFN activity and provide evidence that dietary intervention with SFNmight be protective against NASH.

关键词： Non-alcoholic steatohepatitis(NASH) Krüppel-like factor 4 nuclear translocation Chemokine Lipid metabolism

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Maintaining moderate levels of hypochlorous acid promotes neural stem cell proliferation and differentiation in the recovery phase of stroke

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Neural Regeneration Research 2025年第3期20卷 845-857页

作者： Lin-Yan Huang Yi-De Zhang Jie Chen Hai-Di Fan Wan Wang Bin Wang Ju-Yun Ma Peng-Peng Li Hai-Wei Pu Xin-Yian Guo Jian-Gang Shen Su-Hua Qi School of Medical Technology Xuzhou Key Laboratory of Laboratory DiagnosticsXuzhou Medical UniversityXuzhouJiangsu ProvinceChina School of Pharmacy Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina Department of Laboratory Medicine Branch Hospital of Huai’an First People’s HospitalHuai’anJiangsu ProvinceChina Department of Laboratory Medicine the Affiliated Hospital of Xuzhou Medical UniversityXuzhouJiangsu ProvinceChina School of Chinese Medicine The University of Hong KongHong Kong Special Administrative RegionChina

It has been shown clinically that continuous removal of ischemia/reperfusion-induced reactive oxygen species is not conducive to the recovery of late ***,previous studies have shown that excessive increases in hypochlorous acid after stroke can cause severe damage to brain *** previous studies have found that a small amount of hypochlorous acid still exists in the later stage of stroke,but its specific role and mechanism are currently *** simulate stroke in vivo,a middle cerebral artery occlusion rat model was established,with an oxygen-glucose deprivation/reoxygenation model established in vitro to mimic *** found that in the early stage(within 24 hours)of ischemic stroke,neutrophils produced a large amount of hypochlorous acid,while in the recovery phase(10 days after stroke),microglia were activated and produced a small amount of hypochlorous ***,in acute stroke in rats,hypochlorous acid production was prevented using a hypochlorous acid scavenger,taurine,or myeloperoxidase inhibitor,4-aminobenzoic acid *** results showed that high levels of hypochlorous acid(200μM)induced neuronal apoptosis after oxygen/glucose deprivation/***,in the recovery phase of the middle cerebral artery occlusion model,a moderate level of hypochlorous acid promoted the proliferation and differentiation of neural stem cells into neurons and *** suggests that hypochlorous acid plays different roles at different phases of cerebral ischemia/reperfusion *** levels of hypochlorous acid(5 and 100μM)promoted nuclear translocation ofβ-*** transfection of single-site mutation plasmids,we found that hypochlorous acid induced chlorination of theβ-catenin tyrosine 30 residue,which promoted nuclear ***,our study indicates that maintaining low levels of hypochlorous acid plays a key role in the recovery of neurological function.

关键词： cell differentiation cerebral ischemia/reperfusion injury chlorination hypochlorous acid microglia neural stem cell neurogenesis nuclear translocation stroke β-catenin

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Dihydrotanshinone I preconditions myocardium against ischemic injury via PKM2 glutathionylation sensitive to ROS

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Acta Pharmaceutica Sinica B 2023年第1期13卷 113-127页

作者： Xunxun Wu Lian Liu Qiuling Zheng Hui Ye Hua Yang Haiping Hao Ping Li State Key Laboratory of Natural Medicines Department of PharmacognosySchool of Traditional Chinese PharmacyChina Pharmaceutical UniversityNanjing 210009China College of Pharmacy China Pharmaceutical UniversityNanjing 210009China State Key Laboratory of Natural Medicines Jiangsu Provincial Key Laboratory of Drug Metabolism and PharmacokineticsChina Pharmaceutical UniversityNanjing 210009China

Ischemic preconditioning(IPC)is a potential intervention known to protect the heart against ischemia/reperfusion injury,but its role in the no-reflow phenomenon that follows reperfusion is *** I(DT)is a natural compound and this study illustrates its role in cardiac ischemic injury from the aspect of *** with DT induced modest ROS production and protected cardiomyocytes against oxygen and glucose deprivation(OGD),but the protection was prevented by a ROS *** addition,DT administration protected the heart against isoprenaline ***,PKM2 reacted to transient ROS via oxidization at Cys423/Cys424,leading to glutathionylation and nuclear translocation in dimer *** the nucleus,PKM2 served as a co-factor to promote HIF-1a-dependent gene induction,contributing to adaptive *** mice subjected to permanent coronary ligation,cardiac-specific knockdown of Pkm2 blocked DT-mediated preconditioning protection,which was rescued by overexpression of wild-type Pkm2,rather than Cys423/424-mutated *** conclusion,PKM2 is sensitive to oxidation,and subsequent glutathionylation promotes its nuclear *** IPC has been viewed as a protective means against reperfusion injury,our study reveals its potential role in protection of the heart from no-reflow ischemia.

关键词： Dihydrotanshinone I Ischemic preconditioning PKM2 Glutathionylation Myocardial ischemia ROS Oxidation modification nuclear translocation

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Protocatechuic aldehyde protects cardiomycoytes against ischemic injury via regulation of nuclear pyruvate kinase M2

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Acta Pharmaceutica Sinica B 2021年第11期11卷 3553-3566页

作者： Xunxun Wu Lian Liu Qiuling Zheng Haiping Hao Hui Ye Ping Li Hua Yang State Key Laboratory of Natural Medicines China Pharmaceutical UniversityNanjing 210009China College of Pharmacy China Pharmaceutical UniversityNanjing 210009China Jiangsu Provincial Key Laboratory of Drug Metabolism and Pharmacokinetics China Pharmaceutical UniversityNanjing 210009China

Rescuing cells from stress damage emerges a potential therapeutic strategy to combat myocardial *** aldehyde(PCA)is a major phenolic acid in Chinese herb Danshen(Salvia miltiorrhiza root).This study investigated whether PCA regulated nuclear pyruvate kinase isoform M2(PKM2)function to protect *** rats subjected to isoprenaline,PCA attenuated heart injury and protected cardiomyocytes from *** DARTS and CETSA assays,we identified that PCA bound and promoted PKM2 nuclear translocation in cardiomyocytes exposed to oxygen/glucose deprivation(OGD).In the nucleus,PCA increased the binding of PKM2 to β-Catenin via preserving PKM2 acetylation,and the complex,in cooperation with T-cell factor 4(TCF4),was required for transcriptional induction of genes encoding anti-apoptotic proteins,contributing to rescuing cardiomyocyte *** addition,PCA ameliorated mitochondrial dysfunction and prevented mitochondrial apoptosis dependent on ***,PCA increased the binding of PKM2 to β-Catenin,improved heart contractive function,normalized heart structure and attenuated oxidative damage in mice subjected to artery ligation,but the protective effects were lost in Pkm2-deficient ***,we showed that PCA regulated nuclear PKM2 function to rescue cardiomyocyte survival via β-Catenin/TCF4 signaling cascade,suggesting the potential of pharmacological intervention of PKM2 shuttle to protect the heart.

关键词： Protocatechuic aldehyde PKM2 β-Catenin TCF4 Heart ischemia Myocardial infarction Apoptosis Mitochondrial damage nuclear translocation

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Signaling control of the constitutive androstane receptor(CAR)

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Protein & Cell 2014年第2期5卷 113-123页

作者： Hui Yang Hongbing Wang Department of Pharmaceutical Sciences University of Maryland School of Pharmacy

The constitutive androstane receptor(CAR, NR1I3) plays a crucial role in the regulation of drug metabolism,energy homeostasis, and cancer development through modulating the transcription of its numerous target genes. Different from prototypical nuclear receptors,CAR can be activated by either direct ligand binding or ligand-independent(indirect) mechanisms both initiated with nuclear translocation of CAR from the cytoplasm. In comparison to the well-defined ligand-based activation,indirect activation of CAR appears to be exclusively involved in the nuclear translocation through mechanisms yet to be fully understood. Accumulating evidence reveals that without activation, CAR forms a protein complex in the cytoplasm where it can be functionally affected by multiple signaling pathways. In this review, we discuss recent progresses in our understanding of the signaling regulation of CAR nuclear accumulation and activation. We expect that this review will also provide greater insight into the similarity and difference between the mechanisms of direct vs. indirect human CAR activation.

关键词： constitutive androstane receptor nuclear translocation phosphorylation signaling regulation

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