ArticlePediatric research2006
Separate respiratory phenotypes in methyl-CpG-binding protein 2 (Mecp2) deficient mice.
Article in Pediatric research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 62 citations in OpenAlex.
- Carotid body dysfunction contributes to respiratory instability in Rett syndrome.Current biology : CB · 2026Article
- MeCP2 at the crossroads of hypoxia, oxidative stress, and gene regulation in Rett syndrome.Epigenomics · 2025Review
- Potentiation of the MNeurobiology of disease · 2025Article
- Breathing disturbances in Rett syndrome.Handbook of clinical neurology · 2022Review
- Breathing Abnormalities During Sleep and Wakefulness in Rett Syndrome: Clinical Relevance and Paradoxical Relationship With Circulating Pro-oxidant Markers.Frontiers in neurology · 2022Article
- Loss of MeCP2 Function Across Several Neuronal Populations Impairs Breathing Response to Acute Hypoxia.Frontiers in neurology · 2020Article
- The course of awake breathing disturbances across the lifespan in Rett syndrome.Brain & development · 2018Article
- Breathing abnormalities in animal models of Rett syndrome a female neurogenetic disorder.Respiratory physiology & neurobiology · 2017Review
- Pathogenesis of Lethal Aspiration Pneumonia in Mecp2-null Mouse Model for Rett Syndrome.Scientific reports · 2017Article
- Embryonic hindbrain patterning genes delineate distinct cardio-respiratory and metabolic homeostatic populations in the adult.Scientific reports · 2017Article
- Exclusive expression of MeCP2 in the nervous system distinguishes between brain and peripheral Rett syndrome-like phenotypes.Human molecular genetics · 2016Article
- MeCP2 deficiency results in robust Rett-like behavioural and motor deficits in male and female rats.Human molecular genetics · 2016Article
- Loss of MeCP2 Causes Urological Dysfunction and Contributes to Death by Kidney Failure in Mouse Models of Rett Syndrome.PloS one · 2016Article
- Impaired CO2 sensitivity of astrocytes in a mouse model of Rett syndrome.The Journal of physiology · 2015Article
- Genotype-specific effects of Mecp2 loss-of-function on morphology of Layer V pyramidal neurons in heterozygous female Rett syndrome model mice.Frontiers in cellular neuroscience · 2015Article
- β2-Adrenergic receptor agonist ameliorates phenotypes and corrects microRNA-mediated IGF1 deficits in a mouse model of Rett syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Effect of Sarizotan, a 5-HT1a and D2-like receptor agonist, on respiration in three mouse models of Rett syndrome.American journal of respiratory cell and molecular biology · 2014Article
- Respiratory phenotypes are distinctly affected in mice with common Rett syndrome mutations MeCP2 T158A and R168X.Neuroscience · 2014Article
- Article
- Inflammatory lung disease in Rett syndrome.Mediators of inflammation · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Rett syndrome (RTT) is a neurodevelopmental disorder caused by mutations in the X-linked gene methyl-CpG-binding protein 2 (MECP2) that encodes a DNA binding protein involved in gene silencing. Selective deletion of Mecp2 in post-mitotic neurons in mice results in a Rett-like phenotype characterized by disturbances in motor activity and body weight, suggesting that these symptoms are exclusively caused by neuronal deficiency. Included in the RTT phenotype are episodes of respiratory depression that follow hyperventilation. Here we show that the respiratory phenotype depends on the organ distribution of Mecp2 deficiency. Both female mice heterozygous for a null mutation in Mecp2 (Mecp2+/-) and those with selective deletion of the protein in neurons (Mecp2+/nestin-Cre lox), showed an initial response to hypoxia that exceeded that in wild type (WT). However, marked respiratory depression following hypoxic hyperventilation was only seen in Mecp2+/- animals. Addition of carbon dioxide to the hypoxic exposure eliminated the respiratory depression. Tidal volume and lung volume were larger in Mecp2+/- and respiratory depression was directly related to tidal volume. Taken together these results indicate that the depression is due to hypocapnia. Respiratory depression in this mouse model of Rett Syndrome is seen in with ubiquitous deficiency in Mecp2 but not when it is confined to neurons.
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Registered trials
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.