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<dc:title>Comparative gene expression profile of mouse carotid body and adrenal medulla under physiological hypoxia</dc:title>
<dc:creator>Ganfornina Álvarez, María Dolores</dc:creator>
<dc:creator>Pérez García, María Teresa</dc:creator>
<dc:creator>Gutiérrez, Gabriel</dc:creator>
<dc:creator>Miguel Velado, Eduardo</dc:creator>
<dc:creator>López López, José Ramón</dc:creator>
<dc:creator>Marín, Antonio</dc:creator>
<dc:creator>Sánchez Romero, Diego</dc:creator>
<dc:creator>González Martínez, Constancio</dc:creator>
<dc:subject>Genética</dc:subject>
<dc:description>Producción Científica</dc:description>
<dc:description>The carotid body (CB) is an arterial chemoreceptor, bearing specialized type I cells that respond&#xd;
to hypoxia by closing specific K+ channels and releasing neurotransmitters to activate sensory&#xd;
axons. Despitehaving detailed informationonthe electricalandneurochemicalchangestriggered&#xd;
by hypoxia in CB, the knowledge of the molecular components involved in the signalling cascade&#xd;
of the hypoxic response is fragmentary. This study analyses the mouse CB transcriptional&#xd;
changes in response to low PO2 by hybridization to oligonucleotide microarrays. The transcripts&#xd;
were obtained from whole CBs after mice were exposed to either normoxia (21% O2),&#xd;
or physiological hypoxia (10% O2) for 24 h. The CB transcriptional profiles obtained under&#xd;
these environmental conditions were subtracted fromthe profile of control non-chemoreceptor&#xd;
adrenal medulla extracted from the same animals. Given the common developmental origin of&#xd;
these two organs, they share many properties but differ specifically in their response to O2. Our&#xd;
analysis revealed 751 probe sets regulated specifically in CB under hypoxia (388 up-regulated&#xd;
and 363 down-regulated). These results were corroborated by assessing the transcriptional&#xd;
changesof selectedgenesunderphysiologicalhypoxiawithquantitativeRT-PCR.Ourmicroarray&#xd;
experiments revealed a number of CB-expressed genes (e.g. TH, ferritin and triosephosphate&#xd;
isomerase) that were known to change their expression under hypoxia. However, we also found&#xd;
novel genes that consistently changed their expression under physiological hypoxia. Among&#xd;
them, a group of ion channels show specific regulation in CB: the potassium channels Kir6.1 and&#xd;
Kcnn4 are up-regulated, while the modulatory subunit Kcnab1 is down-regulated by low PO2&#xd;
levels.</dc:description>
<dc:date>2014-09-19T16:44:20Z</dc:date>
<dc:date>2015-09-19T23:40:08Z</dc:date>
<dc:date>2005</dc:date>
<dc:type>info:eu-repo/semantics/article</dc:type>
<dc:identifier>Journal of Physiology, 2005, vol. 566, n. 2, p. 491-503</dc:identifier>
<dc:identifier>0022-3751</dc:identifier>
<dc:identifier>http://uvadoc.uva.es/handle/10324/6100</dc:identifier>
<dc:identifier>10.1113/jphysiol.2005.088815</dc:identifier>
<dc:identifier>491</dc:identifier>
<dc:identifier>2</dc:identifier>
<dc:identifier>503</dc:identifier>
<dc:identifier>Journal of Physiology</dc:identifier>
<dc:identifier>566</dc:identifier>
<dc:language>eng</dc:language>
<dc:rights>info:eu-repo/semantics/embargoedAccess</dc:rights>
<dc:publisher>The Physiological Society</dc:publisher>
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