1
40
2
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/ajpheart.00449.2015" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00449.2015</a>
Pages
H20–28
Issue
1
Volume
310
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Early upregulation of myocardial CXCR4 expression is critical for dimethyloxalylglycine-induced cardiac improvement in acute myocardial infarction.
Publisher
An entity responsible for making the resource available
American journal of physiology. Heart and circulatory physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-01
Subject
The topic of the resource
alpha Subunit/metabolism; Amino Acids; Animal; Animals; Apoptosis/drug effects; Cardiotonic Agents/*pharmacology; Cell Hypoxia; Cell Line; CXCR4/deficiency/genetics/*metabolism; Dicarboxylic/*pharmacology; Disease Models; Enzyme Inhibitors/pharmacology; hypoxia; Hypoxia-Inducible Factor 1; Hypoxia-Inducible Factor-Proline Dioxygenases/antagonists & inhibitors/metabolism; Inbred C57BL; Knockout; Left/*drug effects; Mice; myocardial infarction; Myocardial Infarction/*drug therapy/genetics/metabolism/pathology/physiopathology; Myocardium/*metabolism/pathology; Rats; Receptors; Recovery of Function; Signal Transduction/drug effects; stem cells; Stem Cells/drug effects/metabolism; Stroke Volume/drug effects; Time Factors; Up-Regulation; Ventricular Function
Creator
An entity primarily responsible for making the resource
Mayorga Mari; Kiedrowski Matthew; Shamhart Patricia; Forudi Farhad; Weber Kristal; Chilian William M; Penn Marc S; Dong Feng
Description
An account of the resource
The stromal cell-derived factor-1 (SDF-1):CXCR4 is important in myocardial repair. In this study we tested the hypothesis that early upregulation of cardiomyocyte CXCR4 (CM-CXCR4) at a time of high myocardial SDF-1 expression could be a strategy to engage the SDF-1:CXCR4 axis and improve cardiac repair. The effects of the hypoxia inducible factor (HIF) hydroxylase inhibitor dimethyloxalylglycine (DMOG) on CXCR4 expression was tested on H9c2 cells. In mice a myocardial infarction (MI) was produced in CM-CXCR4 null and wild-type controls. Mice were randomized to receive injection of DMOG (DMOG group) or saline (Saline group) into the border zone after MI. Protein and mRNA expression of CM-CXCR4 were quantified. Echocardiography was used to assess cardiac function. During hypoxia, DMOG treatment increased CXCR4 expression of H9c2 cells by 29 and 42% at 15 and 24 h, respectively. In vivo DMOG treatment increased
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00449.2015" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00449.2015</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
alpha Subunit/metabolism
American journal of physiology. Heart and circulatory physiology
Amino Acids
Animal
Animals
Apoptosis/drug effects
Cardiotonic Agents/*pharmacology
Cell Hypoxia
Cell Line
Chilian William M
CXCR4/deficiency/genetics/*metabolism
Department of Integrative Medical Sciences
Dicarboxylic/*pharmacology
Disease Models
Dong Feng
Enzyme Inhibitors/pharmacology
Forudi Farhad
hypoxia
Hypoxia-Inducible Factor 1
Hypoxia-Inducible Factor-Proline Dioxygenases/antagonists & inhibitors/metabolism
Inbred C57BL
Kiedrowski Matthew
Knockout
Left/*drug effects
Mayorga Mari
Mice
myocardial infarction
Myocardial Infarction/*drug therapy/genetics/metabolism/pathology/physiopathology
Myocardium/*metabolism/pathology
NEOMED College of Medicine
Penn Marc S
Rats
Receptors
Recovery of Function
Shamhart Patricia
Signal Transduction/drug effects
stem cells
Stem Cells/drug effects/metabolism
Stroke Volume/drug effects
Time Factors
Up-Regulation
Ventricular Function
Weber Kristal
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.canlet.2016.05.014" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.canlet.2016.05.014</a>
Pages
131–141
Issue
2
Volume
378
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Lipopolysaccharide supports maintaining the stemness of CD133(+) hepatoma cells through activation of the NF-kappaB/HIF-1alpha pathway.
Publisher
An entity responsible for making the resource available
Cancer letters
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-08
Subject
The topic of the resource
*Cancer stem cells; *Lipopolysaccharide; *Plasticity; *Stemness maintenance; *Tumor microenvironment; AC133 Antigen/genetics/*metabolism; alpha Subunit/genetics/*metabolism; Animals; Antineoplastic Agents – Pharmacodynamics; Antineoplastic Agents/pharmacology; Body Weights and Measures; Carcinoma; Cell Line; Cell Movement – Drug Effects; Cell Movement/drug effects; Cell Physiology; Cell Physiology – Drug Effects; Cell Proliferation/drug effects; Drug Resistance; Gene Expression Regulation; Genes; Genetic Techniques; Hepatocellular; Hepatocellular – Drug Therapy; Hepatocellular – Metabolism; Hepatocellular – Pathology; Hepatocellular/drug therapy/genetics/*metabolism/pathology; Humans; Hypoxia-Inducible Factor 1; Inbred BALB C; Lipopolysaccharides – Pharmacodynamics; Lipopolysaccharides/*pharmacology; Liver Neoplasms; Liver Neoplasms – Drug Therapy; Liver Neoplasms – Metabolism; Liver Neoplasms – Pathology; Liver Neoplasms/drug therapy/genetics/*metabolism/pathology; Male; Mice; Neoplasm; Neoplasm Invasiveness; Neoplastic; Neoplastic Stem Cells/*drug effects/metabolism/pathology; NF-kappa B – Metabolism; NF-kappa B/*metabolism; Nude; Phenotype; Proteins; Proteins – Metabolism; RNA Interference; Signal Transduction – Drug Effects; Signal Transduction/drug effects; Stem Cells – Drug Effects; Stem Cells – Metabolism; Stem Cells – Pathology; Time Factors; Transfection; Tumor Burden; Tumor Microenvironment
Creator
An entity primarily responsible for making the resource
Lai Fo-Bao; Liu Wen-Ting; Jing Ying-Ying; Yu Guo-Feng; Han Zhi-Peng; Yang Xue; Zeng Jian-Xing; Zhang Hang-Jie; Shi Rong-Yu; Li Xiao-Yong; Pan Xiao-Rong; Li Rong; Zhao Qiu-Dong; Wu Meng-Chao; Zhang Ping; Liu Jing-Feng; Wei Li-Xin
Description
An account of the resource
Due to the existence of cancer stem cells (CSCs), persistence and relapse of human hepatocellular carcinoma (HCC) are common after treatment with existing anti-cancer therapies. Emerging evidence indicates that lipopolysaccharide (LPS) plays a crucial role in aggravating HCC, but information about the effect of LPS on CSCs of HCC remains scant. Here, we report that the stemness of CD133(+) CSCs sorted from the human HCC cell line Huh7 was maintained well when cells were cultured with LPS. The reduction of CD133 expression was much lesser in cultured CSCs in the presence of LPS. In response to LPS stimulation, CSCs showed an increase in their activity of clonogenesis and tumorigenesis. LPS also supported maintaining CSC abilities of migration, invasion, and chemo-resistance. Treatment with HIF-1alpha-specific siRNA significantly reduced CD133 expression by CSCs at both mRNA and protein levels. Further, the expression of HIF-1alpha and CD133 was reduced in LPS-stimulated CSCs when the NF-kappaB inhibitor was added to the cell culture. HIF-1alpha-specific siRNA also effectively counteracted the effect of LPS on maintaining CSC abilities of migration and invasion. These data indicate that LPS, an important mediator in the liver tumor microenvironment, supports the maintenance of CSC stemness through signaling of the NF-kappaB/HIF-1alpha pathway. Our current study highlights LPS as a potential target for developing new therapeutic approaches to eliminate CSCs during the treatment of HCC.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.canlet.2016.05.014" target="_blank" rel="noreferrer noopener">10.1016/j.canlet.2016.05.014</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Cancer stem cells
*Lipopolysaccharide
*Plasticity
*Stemness maintenance
*Tumor microenvironment
2016
AC133 Antigen/genetics/*metabolism
alpha Subunit/genetics/*metabolism
Animals
Antineoplastic Agents – Pharmacodynamics
Antineoplastic Agents/pharmacology
Body Weights and Measures
Cancer letters
Carcinoma
Cell Line
Cell Movement – Drug Effects
Cell Movement/drug effects
Cell Physiology
Cell Physiology – Drug Effects
Cell Proliferation/drug effects
Department of Integrative Medical Sciences
Drug Resistance
Gene Expression Regulation
Genes
Genetic Techniques
Han Zhi-Peng
Hepatocellular
Hepatocellular – Drug Therapy
Hepatocellular – Metabolism
Hepatocellular – Pathology
Hepatocellular/drug therapy/genetics/*metabolism/pathology
Humans
Hypoxia-Inducible Factor 1
Inbred BALB C
Jing Ying-Ying
Lai Fo-Bao
Li Rong
Li Xiao-Yong
Lipopolysaccharides – Pharmacodynamics
Lipopolysaccharides/*pharmacology
Liu Jing-Feng
Liu Wen-Ting
Liver Neoplasms
Liver Neoplasms – Drug Therapy
Liver Neoplasms – Metabolism
Liver Neoplasms – Pathology
Liver Neoplasms/drug therapy/genetics/*metabolism/pathology
Male
Mice
NEOMED College of Medicine
Neoplasm
Neoplasm Invasiveness
Neoplastic
Neoplastic Stem Cells/*drug effects/metabolism/pathology
NF-kappa B – Metabolism
NF-kappa B/*metabolism
Nude
Pan Xiao-Rong
Phenotype
Proteins
Proteins – Metabolism
RNA Interference
Shi Rong-Yu
Signal Transduction – Drug Effects
Signal Transduction/drug effects
Stem Cells – Drug Effects
Stem Cells – Metabolism
Stem Cells – Pathology
Time Factors
Transfection
Tumor Burden
Tumor Microenvironment
Wei Li-Xin
Wu Meng-Chao
Yang Xue
Yu Guo-Feng
Zeng Jian-Xing
Zhang Hang-Jie
Zhang Ping
Zhao Qiu-Dong