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Genetic background and transient prenatal disruption of vitamin A signaling determine susceptibility to airway hyperresponsiveness in mice

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE307765 | GEO | 2026/01/28

REPOSITORIES: GEO

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Genetic background and transient prenatal disruption of vitamin A signaling determine susceptibility to airway hyperresponsiveness in mice [scMultiome]

Project description:Airway structural changes and hyperresponsiveness (AHR), hallmarks of asthma, are crucially influenced by genetic variations and adverse exposures. While intrauterine environmental perturbations leading to dysfunctional lung development have been linked to adult pulmonary disease, still little is known about the developmental events leading to these postnatal abnormalities. Here, we provide evidence of genetic background playing a key role in this process. Using A/J and C57BL/6J mice known for their distinct susceptibility to AHR, we show that A/J but not C57BL/6J develop an aberrant airway smooth muscle (SM) program and AHR in adulthood when exposed transiently to a vitamin A/retinoic acid (RA)-disrupted intrauterine environment in vivo by a maternal BMS493 administration. Single nuclei multiomics analysis identified a subpopulation of mesenchymal cells that overactivated TGFβ targets in response to BMS selectively in A/J, but not C57BL/6J, embryonic lungs. These cells, localized to sites of airway SM initiation, exhibited robust BMS-mediated upregulation of SMAD2/3 targets, including regulators of SM program Pdgfra and Tnc, and showed stable cell proportions despite the marked transcriptional rewiring following RA disruption. These findings identify TGFβ-activating mesenchymal cells as a critical niche responsive to RA signaling and reveal how genetic background determines developmental susceptibility to micronutrient perturbations with long-term impact on airway function.

2026-01-28 | GSE307731 | GEO

Genetic background and transient prenatal disruption of vitamin A signaling determine susceptibility to airway hyperresponsiveness in mice [RNA-Seq]

2026-01-28 | GSE307576 | GEO

Genetic background and transient prenatal disruption of vitamin A signaling determine susceptibility to airway hyperresponsiveness in mice

Project description:Genetic background and transient prenatal disruption of vitamin A signaling determine susceptibility to airway hyperresponsiveness in mice

| PRJNA1327287 | ENA

Genetic background and transient prenatal disruption of vitamin A signaling determine susceptibility to airway hyperresponsiveness in mice [scMultiome]

Project description:Genetic background and transient prenatal disruption of vitamin A signaling determine susceptibility to airway hyperresponsiveness in mice [scMultiome]

| PRJNA1327228 | ENA

Genetic background and transient prenatal disruption of vitamin A signaling determine susceptibility to airway hyperresponsiveness in mice [RNA-Seq]

Project description:Genetic background and transient prenatal disruption of vitamin A signaling determine susceptibility to airway hyperresponsiveness in mice [RNA-Seq]

| PRJNA1322313 | ENA

Prenatal retinoid deficiency leads to airway hyperresponsiveness in adult mice.

Project description:There is increasing evidence that vitamin A deficiency in utero correlates with abnormal airway smooth muscle (SM) function in postnatal life. The bioactive vitamin A metabolite retinoic acid (RA) is essential for formation of the lung primordium; however, little is known about the impact of early fetal RA deficiency on postnatal lung structure and function. Here, we provide evidence that during murine lung development, endogenous RA has a key role in restricting the airway SM differentiation program during airway formation. Using murine models of pharmacological, genetic, and dietary vitamin A/RA deficiency, we found that disruption of RA signaling during embryonic development consistently resulted in an altered airway SM phenotype with markedly increased expression of SM markers. The aberrant phenotype persisted postnatally regardless of the adult vitamin A status and manifested as structural changes in the bronchial SM and hyperresponsiveness of the airway without evidence of inflammation. Our data reveal a role for endogenous RA signaling in restricting SM differentiation and preventing precocious and excessive SM differentiation when airways are forming.

| S-EPMC3904614 | biostudies-literature

Infants born during COVID-19 pandemic experience increased susceptibility to airway hyperresponsiveness.

Project description:BackgroundAsthma, allergic rhinitis, atopic dermatitis, and food allergy are type 2 inflammation diseases. Since the 1960s, the prevalence of those diseases has steadily increased, presumably due to the "Hygiene hypothesis" which suggests that early exposure of infants to pathogens, siblings, and environmental dust, has a protective effect against the development of allergic diseases. The COVID-19 pandemic increased environmental hygiene due to lockdowns, masks, and social distancing.ObjectiveTo compare the prevalence of allergic diseases among children born before and during the pandemic.MethodsThe Cow's Milk Early Exposure Trial prospectively followed newborns until 12-months of age using monthly survey and examined milk allergy development. Some were born before the first COVID-19 lockdown in Israel (April 2018-March 2020), and some were born during the pandemic (March 2020-May 2021). The monthly surveys included questions regarding atopic comorbidities.ResultsA total of 1,989 infants completed 12-months of follow-up. Among them, 1,086(54.5%) were diagnosed with at least one atopic disease. Among 235 infants born after the last lockdown, 162 were diagnosed with airway hyperresponsiveness (AHR)(68.9%), significantly more than in any other group. No other significant differences were found between the study groups.ConclusionsThere was no significant difference in the development of atopic comorbidities between infants born before and during the pandemic. Significantly more infants who were born after restrictions were eased were diagnosed AHR. A longer follow-up period is needed to obtain a better understanding of the influence of the COVID-19 restrictions on the development of atopic comorbidities.Clinical trial registryNIH Clinical Trials Registry: NCT02785679.

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Murine Airway Hyperresponsiveness

Project description:This project investigates the mechanisms that underlie asthma-related phenotypes associated with allergen exposure. See http://www.hopkins-genomics.org/asthma/asthma006/index.html The goal of the experiment was to identify genes that change their levels of expression as a consequence of challenge with allergen. The experiments utilized a murine model of human asthma that employed BALB/CJ mice. In this particular sensitization-challenge protocol, the response produced by BALB/CJ mice is representative of a majority of the mouse strains tested. The antigen complex used to sensitize and challenge the mice was ragweed pollen an allergen that is highly relevant to human disease. Keywords: time series, allergen

2005-08-24 | GSE3184 | GEO

Human Airway Hyperresponsiveness

Project description:The purpose of this project is to gain a better understanding of the early cytokine-mediated mechanisms that lead to asthma. Keywords: time series, IL13

2005-08-24 | GSE3183 | GEO

Multistrain genetic comparisons reveal CCR5 as a receptor involved in airway hyperresponsiveness.

Project description:Asthma is a ubiquitous disease with a broad range of clinical phenotypes. To better understand the complex genetic and environmental interactions underlying asthma, we compared the gene-gene interactions of four genetically distinct mouse strains that demonstrate biologically distinct responses to allergen. Using DNA microarrays and knock-out mouse studies, we showed that CCR5 plays a definitive role in the development of ovalbumin-induced allergic airway inflammatory disease. In addition, gene expression profiling data have revealed other potential novel targets for therapeutics-based research and has enhanced the understanding of the molecular mechanisms underlying the etiology of "asthma."

| S-EPMC2644233 | biostudies-literature

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