RT info:eu-repo/semantics/article
T1 Comparative gene expression profile of mouse carotid body and adrenal medulla under physiological hypoxia
A1 Ganfornina Álvarez, María Dolores
A1 Pérez García, María Teresa
A1 Gutiérrez, Gabriel
A1 Miguel Velado, Eduardo
A1 López López, José Ramón
A1 Marín, Antonio
A1 Sánchez Romero, Diego
A1 González, Constancio
K1 Genética
AB The carotid body (CB) is an arterial chemoreceptor, bearing specialized type I cells that respondto hypoxia by closing specific K+ channels and releasing neurotransmitters to activate sensoryaxons. Despitehaving detailed informationonthe electricalandneurochemicalchangestriggeredby hypoxia in CB, the knowledge of the molecular components involved in the signalling cascadeof the hypoxic response is fragmentary. This study analyses the mouse CB transcriptionalchanges in response to low PO2 by hybridization to oligonucleotide microarrays. The transcriptswere 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 underthese environmental conditions were subtracted fromthe profile of control non-chemoreceptoradrenal medulla extracted from the same animals. Given the common developmental origin ofthese two organs, they share many properties but differ specifically in their response to O2. Ouranalysis revealed 751 probe sets regulated specifically in CB under hypoxia (388 up-regulatedand 363 down-regulated). These results were corroborated by assessing the transcriptionalchangesof selectedgenesunderphysiologicalhypoxiawithquantitativeRT-PCR.Ourmicroarrayexperiments revealed a number of CB-expressed genes (e.g. TH, ferritin and triosephosphateisomerase) that were known to change their expression under hypoxia. However, we also foundnovel genes that consistently changed their expression under physiological hypoxia. Amongthem, a group of ion channels show specific regulation in CB: the potassium channels Kir6.1 andKcnn4 are up-regulated, while the modulatory subunit Kcnab1 is down-regulated by low PO2levels.
PB The Physiological Society
SN 0022-3751
YR 2005
FD 2005
LK http://uvadoc.uva.es/handle/10324/6100
UL http://uvadoc.uva.es/handle/10324/6100
LA eng
NO Journal of Physiology, 2005, vol. 566, n. 2, p. 491-503
NO Producción Científica
DS UVaDOC
RD 18-dic-2024