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/ajpcell.00068.2016" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpcell.00068.2016</a>
Pages
C212–224
Issue
2
Volume
311
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
Leptin augments recruitment of IRF-1 and CREB to thrombospondin-1 gene promoter in vascular smooth muscle cells in vitro.
Publisher
An entity responsible for making the resource available
American journal of physiology. Cell physiology
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
*cAMP response element-binding protein; *interferon regulatory factor-1; *leptin; *thrombospondin-1; *transcription; *vascular smooth muscle cells; Binding Sites/genetics; Cells; Chromatin Immunoprecipitation/methods; Cultured; Cyclic AMP Response Element-Binding Protein/*metabolism; Gene Expression Regulation/genetics; Genetic/genetics; Humans; Interferon Regulatory Factor-1/*metabolism; Leptin/*metabolism; Muscle; Mutagenesis; Myocytes; Promoter Regions; Response Elements/genetics; Site-Directed/methods; Smooth; Smooth Muscle/*metabolism; Thrombospondin 1/*genetics/*metabolism; Transcription; Transcriptional Activation/genetics; Transfection/methods; Up-Regulation/genetics; Vascular/*metabolism
Creator
An entity primarily responsible for making the resource
Sahu Soumyadip; Ganguly Rituparna; Raman Priya
Description
An account of the resource
We previously reported that high pathophysiological concentrations of leptin, the adipocyte-secreted peptide, upregulate the expression of a potent proatherogenic matricellular protein, thrombospondin-1 (TSP-1), in vascular smooth muscle cells. Moreover, this regulation was found to occur at the level of transcription; however, the underlying molecular mechanisms remain unknown. The goal of the present study was to investigate the specific transcriptional mechanisms that mediate upregulation of TSP-1 expression by leptin. Primary human aortic smooth muscle cell cultures were transiently transfected with different TSP-1 gene (THBS1) promoter-linked luciferase reporter constructs, and luciferase activity in response to leptin (100 ng/ml) was assessed. We identified a long THBS1 promoter (-1270/+750) fragment with specific leptin response elements that are required for increased TSP-1 transcription by leptin. Promoter analyses, protein/DNA array and gel shift assays demonstrated activation and association of transcription factors, interferon regulatory factor-1 (IRF-1) and cAMP response element-binding protein (CREB), to the distal fragment of the THBS1 promoter in response to leptin. Supershift, chromatin immunoprecipitation, and coimmunoprecipitation assays revealed formation of a single complex between IRF-1 and CREB in response to leptin; importantly, recruitment of this complex to the THBS1 promoter mediated leptin-induced TSP-1 transcription. Finally, binding sequence decoy oligomer and site-directed mutagenesis revealed that regulatory elements for both IRF-1 (-1019 to -1016) and CREB (-1198 to -1195), specific to the distal THBS1 promoter, were required for leptin-induced TSP-1 transcription. Taken together, these findings demonstrate that leptin promotes a cooperative association between IRF-1 and CREB on the THBS1 promoter driving TSP-1 transcription in vascular smooth muscle cells.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpcell.00068.2016" target="_blank" rel="noreferrer noopener">10.1152/ajpcell.00068.2016</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*cAMP response element-binding protein
*interferon regulatory factor-1
*leptin
*thrombospondin-1
*Transcription
*vascular smooth muscle cells
2016
American journal of physiology. Cell physiology
Binding Sites/genetics
Cells
Chromatin Immunoprecipitation/methods
Cultured
Cyclic AMP Response Element-Binding Protein/*metabolism
Department of Integrative Medical Sciences
Ganguly Rituparna
Gene Expression Regulation/genetics
Genetic/genetics
Humans
Interferon Regulatory Factor-1/*metabolism
Leptin/*metabolism
Muscle
Mutagenesis
Myocytes
NEOMED College of Medicine
Promoter Regions
Raman Priya
Response Elements/genetics
Sahu Soumyadip
Site-Directed/methods
Smooth
Smooth Muscle/*metabolism
Thrombospondin 1/*genetics/*metabolism
Transcription
Transcriptional Activation/genetics
Transfection/methods
Up-Regulation/genetics
Vascular/*metabolism
-
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/10.1186/s13041-018-0376-5" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/s13041-018-0376-5</a>
Pages
34–34
Issue
1
Volume
11
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
RNAseq analysis of hippocampal microglia after kainic acid-induced seizures.
Publisher
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Molecular brain
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-06
Subject
The topic of the resource
Animals; Gene Expression Profiling; Gene Ontology; Hippocampus/*pathology; Immunity; Interferon-beta/metabolism; Kainic Acid; Mice; Microglia/*metabolism/*pathology; RNA/*methods; Seizures/*chemically induced; Sequence Analysis; Signal Transduction/genetics; Up-Regulation/genetics
Creator
An entity primarily responsible for making the resource
Bosco Dale B; Zheng Jiaying; Xu Zhiyan; Peng Jiyun; Eyo Ukpong B; Tang Ke; Yan Cheng; Huang Jun; Feng Lijie; Wu Gongxiong; Richardson Jason R; Wang Hui; Wu Long-Jun
Description
An account of the resource
Microglia have been shown to be of critical importance to the progression of temporal lobe epilepsy. However, the broad transcriptional changes that these cells undergo following seizure induction is not well understood. As such, we utilized RNAseq analysis upon microglia isolated from the hippocampus to determine expression pattern alterations following kainic acid induced seizure. We determined that microglia undergo dramatic changes to their expression patterns, particularly with regard to mitochondrial activity and metabolism. We also observed that microglia initiate immunological activity, specifically increasing interferon beta responsiveness. Our results provide novel insights into microglia transcriptional regulation following acute seizures and suggest potential therapeutic targets specifically in microglia for the treatment of seizures and epilepsy.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1186/s13041-018-0376-5" target="_blank" rel="noreferrer noopener">10.1186/s13041-018-0376-5</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).
2018
Animals
Bosco Dale B
Department of Pharmaceutical Sciences
Eyo Ukpong B
Feng Lijie
Gene Expression Profiling
Gene Ontology
Hippocampus/*pathology
Huang Jun
Immunity
Interferon-beta/metabolism
Kainic Acid
Mice
Microglia/*metabolism/*pathology
Molecular brain
NEOMED College of Pharmacy
Peng Jiyun
Richardson Jason R
RNA/*methods
Seizures/*chemically induced
Sequence Analysis
Signal Transduction/genetics
Tang Ke
Up-Regulation/genetics
Wang Hui
Wu Gongxiong
Wu Long-Jun
Xu Zhiyan
Yan Cheng
Zheng Jiaying