| AHR, a novel acute hypoxia-response sequence, drives reporter gene expression under hypoxia in vitro and in vivo. | |
| | |
MedLine Citation:
|
PMID: 20795945 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
ADAMTS1 (a disintegrin and metalloproteinase with thrombospondin motifs 1) is an early immediate gene. We have previously reported that ADAMTS1 was strongly induced by hypoxia. In this study, we investigated whether ADAMTS1 promoter-driven reporter signal is detectable by acute hypoxia. We constructed the GFP (green fluorescent protein) expression vector [AHR (acute hypoxia-response sequence)-GFP] under the control of ADAMTS1 promoter and compared it with the constitutive GFP-expressing vector under the control of CMV (cytomegalovirus promoter-GFP). We transduced AHR-GFP and examined whether GFP signals can be detected under the acute hypoxia. When the human umbilical vein [HUVEC (human umbilical vein endothelial cells)] was transduced under normoxia, there were few GFP signals, while CMV-GFP showed considerable GFP signals. When HUVEC was stimulated with hypoxia, GFP signals from AHR-GFP gene were induced under hypoxic conditions. Notably, the GFP signals peaked at 3 h under hypoxia. In ischaemic hind limb model, transduced AHR-GFP showed hypoxic induction of GFP signals. In summary, we have demonstrated that the AHR system induced the reporter gene expression by acute hypoxia, and its induction is transient. This is the first report showing the unique acute hypoxia-activated gene expression system. |
| | |
Authors:
|
Mehmet Zeynel Cilek; Satoshi Hirohata; Omer Faruk Hatipoglu; Hiroko Ogawa; Toru Miyoshi; Junko Inagaki; Takashi Ohtsuki; Hiroshi Harada; Shigeshi Kamikawa; Shozo Kusachi; Yoshifumi Ninomiya |
Related Documents
:
|
9782295 - Construction of a mouse hepatitis virus recombinant expressing a foreign gene. 15838265 - Localization of the endothelin-b receptor using a transgenic approach. 15483665 - Efficient and stable sendai virus-mediated gene transfer into primate embryonic stem ce... 10712585 - Quantitative analysis of gene expression with an improved green fluorescent protein. p6. 20231365 - The gene for aromatase, a rate-limiting enzyme for local estrogen biosynthesis, is a do... 21415115 - Function of the bacteriophytochrome bphp in the rpos/las-quorum sensing network of pseu... |
Publication Detail:
|
Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
|
Title: Cell biology international Volume: 35 ISSN: 1095-8355 ISO Abbreviation: Cell Biol. Int. Publication Date: 2011 Jan |
Date Detail:
|
Created Date: 2010-12-01 Completed Date: 2011-03-08 Revised Date: 2011-04-08 |
Medline Journal Info:
|
Nlm Unique ID: 9307129 Medline TA: Cell Biol Int Country: England |
Other Details:
|
Languages: eng Pagination: 1-8 Citation Subset: IM |
Affiliation:
|
Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
ADAM Proteins
/
biosynthesis,
genetics* Animals Cell Hypoxia Cells, Cultured Endothelial Cells / metabolism Endothelium, Vascular / metabolism Gene Expression Regulation Genes, Reporter Green Fluorescent Proteins / biosynthesis, genetics Hindlimb Humans Hypoxia-Inducible Factor 1 / genetics, metabolism Ischemia / metabolism Mice Mice, Inbred C57BL Muscle, Skeletal / blood supply, metabolism Promoter Regions, Genetic RNA, Messenger / biosynthesis |
| Chemical | |
Reg. No./Substance:
|
0/Hypoxia-Inducible Factor 1; 0/RNA, Messenger; 147336-22-9/Green Fluorescent Proteins; EC 3.4.24.-/ADAM Proteins; EC 3.4.24.-/ADAMTS1 protein, human; EC 3.4.24.-/Adamts1 protein, mouse |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Overexpression of amyloid beta precursor protein enhances expression and secretion of ST6Gal1 in C2C...
Next Document: Sitagliptin prevents the development of metabolic and hormonal disturbances, increased ?-cell apopto...