The human carotid body transcriptome with focus on oxygen sensing and inflammation-a comparative analysis

et al.The carotid body (CB) is the key oxygen sensing organ. While the expression of CB specific genes is relatively well studied in animals, corresponding data for the human CB are missing. In this study we used five surgically removed human CBs to characterize the CB transcriptome with microarray and PCR analyses, and compared the results with mice data. In silico approaches demonstrated a unique gene expression profile of the human and mouse CB transcriptomes and an unexpected upregulation of both human and mouse CB genes involved in the inflammatory response compared to brain and adrenal gland data. Human CBs express most of the genes previously proposed to be involved in oxygen sensing and signalling based on animal studies, including NOX2, AMPK, CSE and oxygen sensitive K+ channels. In the TASK subfamily of K+ channels, TASK-1 is expressed in human CBs, while TASK-3 and TASK-5 are absent, although we demonstrated both TASK-1 and TASK-3 in one of the mouse reference strains. Maxi-K was expressed exclusively as the spliced variant ZERO in the human CB. In summary, the human CB transcriptome shares important features with the mouse CB, but also differs significantly in the expression of a number of CB chemosensory genes. This study provides key information for future functional investigations on the human carotid body. © 2012 The Authors. The Journal of Physiology © 2012 The Physiological Society.This work was supported by grants from the Swedish Research Council (No. 521-2011-152 (L.I.E.)), the Stockholm County Council (ALF project 20090321 (L.I.E.)), Post-Doc project 108042 (M.J.F.), Karolinska Foundations (M.J.F., L.I.E.), The Swedish Society of Medicine (L.I.E.), LPS Medical Foundation (M.J.F.), and Fraenkel Foundation (M.J.F., L.I.E.). C.G. is supported by the Ministerio de Ciencia e Innovación of Spain, grant no. BFU2007-61848, and by the Instituto Carlos III, grant no. CIBER CB06/06/0050. D.S. is supported by the MICINN grant BFU2008-01170. E.W.K. and M.S. are supported by NHLBI HL81345 of the USA.Peer Reviewe