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Cystic fibrosis causes olfactory system defects by altering progenitor cell proliferation

ABSTRACT: Cystic fibrosis causes olfactory system defects by altering progenitor cell proliferation

PROVIDER: PRJNA809332 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18099334.fastq.gz	Fastqsanger.gz
	SRR18099335.fastq.gz	Fastqsanger.gz
	SRR18099336.fastq.gz	Fastqsanger.gz
	SRR18099337.fastq.gz	Fastqsanger.gz
	SRR18099338.fastq.gz	Fastqsanger.gz

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Cystic fibrosis causes olfactory system defects by altering progenitor cell proliferation (scRNA-Seq)

Project description:A reduced sense of smell has been reported in people with cystic fibrosis (CF). These olfactory defects have largely been attributed to secondary manifestations of the disease, such as inflammation of the nasal mucosa. Here we show that CFTR, the gene responsible for CF, is expressed in proliferating olfactory human cells and that newborn CFTR null pigs display ultrastructural abnormalities in the olfactory epithelium and olfactory bulbs. In the absence of CFTR, olfactory sensory neurons still produce odor-evoked activity, but mutant animals display defective odor-guided suckling behavior after birth. Consistent with epithelial changes, we found a reduced expression of genes implicated in cell cycle and development in globose basal cells (GBCs), the neurogenic progenitor cells in the olfactory epithelium. Targeted sequencing revealed enhanced CFTR expression in the subpopulation of GBCs that is actively proliferating. Furthermore, CFTR loss caused a global reduction in the number of sensory neurons and altered olfactory receptors expression. Our findings highlight a previously unknown role of CFTR in olfactory system function by regulating progenitor cell proliferation in the olfactory epithelium.

2022-12-31 | GSE197189 | GEO

Cystic fibrosis causes olfactory system defects by altering progenitor cell proliferation (Bulk RNA-Seq)

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Cystic fibrosis causes olfactory system defects by altering progenitor cell proliferation (scRNA-Seq)

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Cystic fibrosis causes olfactory system defects by altering progenitor cell proliferation (Bulk RNA-Seq)

Project description:Cystic fibrosis causes olfactory system defects by altering progenitor cell proliferation (Bulk RNA-Seq)

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Cystic fibrosis causes olfactory system defects by altering progenitor cell proliferation

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Project description:This multi-center study will compare multi-target DNA and quantitative FIT stool-based testing to colonoscopy in individuals with Cystic Fibrosis (CF) undergoing colon cancer screening with colonoscopy. The primary endpoint is detection of any adenomas, including advanced adenomas and colorectal cancer (CRC).

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Project description:CF's physiopathology is poorly explained by the mutation alone. The oxydative stress could be a major factor of this illness . Study its impact on transcriptome's CF cell line could be ameliorate our understanding of the evolution of cystic fibrosis. we used microarray technology to evaluate under oxydative stress, the transcriptional state of an epithelial lung cell issued from a human with cystic fibrosis and to identify a set of modulated genes associated to survival cell processes.

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SARS-CoV-2 infection causes transient olfactory dysfunction in mice

Project description:SARS-CoV-2 infection causes a wide spectrum of clinical manifestations in human, and olfactory dysfunction represents as one of the most predictive and common symptoms in COVID-19 patients. However, the underlying mechanism how SARS-CoV-2 infection leads to olfactory disorders remains elusive. Herein we demonstrate intranasal inoculation of SARS-CoV-2 induces robust viral replication in the olfactory epithelium (OE), not olfactory bulb (OB), resulting in transient olfactory dysfunction in humanized ACE2 mice. The sustentacular cells and Bowman's gland cells in the OE were identified as the major target cells of SARS-CoV-2 before the invasion into olfactory sensory neurons. Remarkably, SARS-CoV-2 infection triggers massive cell death and immune cell infiltration, and directly impairs the uniformity of OE structure. Combined transcriptomic and quantitative proteomic analyses reveal the induction of antiviral and inflammatory responses, as well as the downregulation of olfactory receptor (OR) genes in the OE from the infected animals. Overall, our mouse model recapitulates the olfactory dysfunction in COVID-19 patients, and provides critical clues to understand the physiological basis for extrapulmonary manifestations of COVID-19.

2021-06-22 | PXD026854 |

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