Physiol. Genomics Journal of Neurophysiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Physiol. Genomics 25: 435-449, 2006. First published February 28, 2006; doi:10.1152/physiolgenomics.00315.2005
1094-8341/06 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental Tables
Right arrow All Versions of this Article:
25/3/435    most recent
00315.2005v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (13)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mense, S. M.
Right arrow Articles by Zhang, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mense, S. M.
Right arrow Articles by Zhang, L.
Received 20 December 2005; accepted in final form 22 February 2006.
Physiological Genomics 25:435-449 (2006)
1094-8341/06 $8.00 © 2006 American Physiological Society

Gene expression profiling reveals the profound upregulation of hypoxia-responsive genes in primary human astrocytes

S. M. Mense 1, A. Sengupta 1, M. Zhou 1, C. Lan 1, G. Bentsman 2, D. J. Volsky 2 and L. Zhang 1

1 Department of Environmental Health Sciences, Mailman School of Public Health
2 Molecular Virology Division, St. Luke’s-Roosevelt Hospital Center and College of Physicians and Surgeons, Columbia University, New York, New York

Oxygen is vital for the development and survival of mammals. In response to hypoxia, the brain initiates numerous adaptive responses at the organ level as well as at the molecular and cellular levels, including the alteration of gene expression. Astrocytes play critical roles in the proper functioning of the brain; thus the manner in which astrocytes respond to hypoxia is likely important in determining the outcome of brain hypoxia. Here, we used microarray gene expression profiling and data-analysis algorithms to identify and analyze hypoxia-responsive genes in primary human astrocytes. We also compared gene expression patterns in astrocytes with those in human HeLa cells and pulmonary artery endothelial cells (ECs). Remarkably, in astrocytes, five times as many genes were induced as suppressed, whereas in HeLa and pulmonary ECs, as many as or more genes were suppressed than induced. More genes encoding hypoxia-inducible functions, such as glycolytic enzymes and angiogenic growth factors, were strongly induced in astrocytes compared with HeLa cells. Furthermore, gene ontology and computational algorithms revealed that many target genes of the EGF and insulin signaling pathways and the transcriptional regulators Myc, Jun, and p53 were selectively altered by hypoxia in astrocytes. Indeed, Western blot analysis confirmed that two major signal transducers mediating insulin and EGF action, Akt and MEK1/2, were activated by hypoxia in astrocytes. These results provide a global view of the signaling and regulatory network mediating oxygen regulation in human astrocytes.

microarray; hypoxic response; signaling pathways




This article has been cited by other articles:


Home page
Nucleic Acids ResHome page
K. Tsuchihara, Y. Suzuki, H. Wakaguri, T. Irie, K. Tanimoto, S.-i. Hashimoto, K. Matsushima, J. Mizushima-Sugano, R. Yamashita, K. Nakai, et al.
Massive transcriptional start site analysis of human genes in hypoxia cells
Nucleic Acids Res., April 1, 2009; 37(7): 2249 - 2263.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
S. Beyer, M. M. Kristensen, K. S. Jensen, J. V. Johansen, and P. Staller
The Histone Demethylases JMJD1A and JMJD2B Are Transcriptional Targets of Hypoxia-inducible Factor HIF
J. Biol. Chem., December 26, 2008; 283(52): 36542 - 36552.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
R. Trollmann, K. Strasser, S. Keller, X. Antoniou, B. Grenacher, O. O. Ogunshola, J. Dotsch, W. Rascher, and M. Gassmann
Placental HIFs as markers of cerebral hypoxic distress in fetal mice
Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2008; 295(6): R1973 - R1981.
[Abstract] [Full Text] [PDF]


Home page
Mol. Biol. CellHome page
J. Kim, Y. Shao, S. Y. Kim, S. Kim, H. K. Song, J. H. Jeon, H. W. Suh, J. W. Chung, S. R. Yoon, Y. S. Kim, et al.
Hypoxia-induced IL-18 Increases Hypoxia-inducible Factor-1{alpha} Expression through a Rac1-dependent NF-{kappa}B Pathway
Mol. Biol. Cell, February 1, 2008; 19(2): 433 - 444.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
A. D. Nguyen, J. G. McDonald, R. K. Bruick, and R. A. DeBose-Boyd
Hypoxia Stimulates Degradation of 3-Hydroxy-3-methylglutaryl-coenzyme A Reductase through Accumulation of Lanosterol and Hypoxia-Inducible Factor-mediated Induction of Insigs
J. Biol. Chem., September 14, 2007; 282(37): 27436 - 27446.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2006 by the American Physiological Society.