2026-05-05T12:29:57Zhttps://uvadoc.uva.es/oai/request

oai:uvadoc.uva.es:10324/61002025-03-03T10:20:11Zcom_10324_32522com_10324_952com_10324_894com_10324_43677com_10324_954com_10324_1134com_10324_931col_10324_32523col_10324_43678col_10324_1213

Ganfornina Álvarez, María Dolores Pérez García, María Teresa Gutiérrez, Gabriel Miguel Velado, Eduardo López López, José Ramón Marín, Antonio Sánchez Romero, Diego González Martínez, Constancio Genética Producción Científica 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. Despitehaving detailed informationonthe electricalandneurochemicalchangestriggered 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 fromthe 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 changesof selectedgenesunderphysiologicalhypoxiawithquantitativeRT-PCR.Ourmicroarray 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. 2014-09-19 2015-09-19 2005 info:eu-repo/semantics/article Journal of Physiology, 2005, vol. 566, n. 2, p. 491-503 0022-3751 http://uvadoc.uva.es/handle/10324/6100 10.1113/jphysiol.2005.088815 491 2 503 Journal of Physiology 566 eng info:eu-repo/semantics/embargoedAccess The Physiological Society