| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Departamento de Bioquímica y Fisiología y Genética Molecular-IBGM, Universidad de Valladolid-CSIC, 47005 Valladolid, Spain
2 Departamento de Genética, Universidad de Sevilla, 41080 Sevilla, Spain
The carotid body (CB) is an arterial chemoreceptor, bearing specialized type I cells that respond to hypoxia by closing specific K+ channels and releasing neurotransmitters to activate sensory axons. Despite having detailed information on the electrical and neurochemical changes triggered by hypoxia in CB, the knowledge of the molecular components involved in the signalling cascade of the hypoxic response is fragmentary. This study analyses the mouse CB transcriptional changes in response to low PO2 by hybridization to oligonucleotide microarrays. The transcripts were obtained from whole CBs after mice were exposed to either normoxia (21% O2), or physiological hypoxia (10% O2) for 24 h. The CB transcriptional profiles obtained under these environmental conditions were subtracted from the profile of control non-chemoreceptor adrenal medulla extracted from the same animals. Given the common developmental origin of these two organs, they share many properties but differ specifically in their response to O2. Our analysis revealed 751 probe sets regulated specifically in CB under hypoxia (388 up-regulated and 363 down-regulated). These results were corroborated by assessing the transcriptional changes of selected genes under physiological hypoxia with quantitative RT-PCR. Our microarray experiments revealed a number of CB-expressed genes (e.g. TH, ferritin and triosephosphate isomerase) that were known to change their expression under hypoxia. However, we also found novel genes that consistently changed their expression under physiological hypoxia. Among them, a group of ion channels show specific regulation in CB: the potassium channels Kir6.1 and Kcnn4 are up-regulated, while the modulatory subunit Kcnab1 is down-regulated by low PO2 levels.
(Received 18 April 2005;
accepted after revision 2 May 2005;
first published online 12 May 2005)
Corresponding author D. Sánchez: Departamento de Bioquímica y Biología Molecular y Fisiología, Facultad de Medicina, C/Ramón y Cajal, 7, Universidad de Valladolid, 47005 Valladolid, Spain. Email: lazarill{at}ibgm.uva.es
This article has been cited by other articles:
|
|
 |
|
  A. Balbir, H. Lee, M. Okumura, S. Biswal, R. S. Fitzgerald, and M. Shirahata A search for genes that may confer divergent morphology and function in the carotid body between two strains of mice Am J Physiol Lung Cell Mol Physiol, March 1, 2007; 292(3): L704 - L715. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Acker, J. Fandrey, and H. Acker The good, the bad and the ugly in oxygen-sensing: ROS, cytochromes and prolyl-hydroxylases Cardiovasc Res, July 15, 2006; 71(2): 195 - 207. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Tajima, K. Schonherr, S. Niedling, M. Kaatz, H. Kanno, R. Schonherr, and S. H. Heinemann Ca2+-activated K+ channels in human melanoma cells are up-regulated by hypoxia involving hypoxia-inducible factor-1{alpha} and the von Hippel-Lindau protein J. Physiol., March 1, 2006; 571(2): 349 - 359. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
