ArticleThe Journal of physiology2005
Comparative gene expression profile of mouse carotid body and adrenal medulla under physiological hypoxia.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 43 citations in OpenAlex.
- Genetic map of the carotid body stem cell niche with focus on the OScientific reports · 2025Article
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- Transcriptomics of the Carotid Body.Advances in experimental medicine and biology · 2023Review
- Article
- Lessons from single-cell transcriptome analysis of oxygen-sensing cells.Cell and tissue research · 2018Review
- Gene expression analyses reveal metabolic specifications in acute OThe Journal of physiology · 2017Article
- Single cell transcriptome analysis of mouse carotid body glomus cells.The Journal of physiology · 2016Article
- KATP Channels in the Cardiovascular System.Physiological reviews · 2016Review
- Article
- Genome wide expression analysis suggests perturbation of vascular homeostasis during high altitude pulmonary edema.PloS one · 2014Article
- The human carotid body transcriptome with focus on oxygen sensing and inflammation--a comparative analysis.The Journal of physiology · 2012Article
- Molecular mechanisms of chronic intermittent hypoxia and hypertension.Critical reviews in biomedical engineering · 2012Review
- Upregulation of transcription factor NRF2-mediated oxidative stress response pathway in rat brain under short-term chronic hypobaric hypoxia.Functional & integrative genomics · 2011Article
- Short-term hypoxia increases tyrosine hydroxylase immunoreactivity in rat carotid body.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2010Article
- Hypoxic transcription gene profiles under the modulation of nitric oxide in nuclear run on-microarray and proteomics.BMC genomics · 2009Article
- Purines, the carotid body and respiration.Respiratory physiology & neurobiology · 2007Review
- Ca2+-activated K+ channels in human melanoma cells are up-regulated by hypoxia involving hypoxia-inducible factor-1alpha and the von Hippel-Lindau protein.The Journal of physiology · 2006Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.