Gene expression profiles in human nasal polyp tissues studied by means of DNA microarray

Zheng, Liduan; Kim, Jean; Sypek, Joseph P.; Wang, I‐Ming; Horton, Heidi F.; Oppenheim, Frank G.; Bochner, Bruce S.

doi:10.1016/j.jaci.2004.04.052

Cited by 109 publications

(135 citation statements)

References 40 publications

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“…It has been demonstrated that CC10 is expressed in the goblet, non-mucinous and non-ciliated cells of the nasal sinus mucosa epithelium and that the number of CC10-positive cells is negatively correlated with inflammatory cell infiltration and the number of goblet cells. This indicates that downregulation of CC10 expression may lead to anti-inflammatory network dysfunction in the epithelial cells of the upper respiratory tract and a persistent severe inflammatory response eventually leads to the formation of NP (9). CC10 expression is negatively correlated with preoperative CT scores, as well as postoperative nasal endoscopy and symptom scores (8).…”

Section: Discussionmentioning

confidence: 99%

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Expression of Clara cell 10-kDa protein and trefoil factor family 1 in patients with chronic rhinosinusitis and nasal polyps

Wang

2018

Exp Ther Med

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Abstract. The current study measured the expression of Clara cell 10-kDa protein (CC10) and trefoil factor family 1 (TFF1) in the sinus mucosa of patients exhibiting chronic rhinosinusitis (CRS) and nasal polyps (NP). CC10 and TFF1 expression in the sinus mucosa of the control group and patients with CRS and NP was determined using reverse transcription-quantitative polymerase chain reaction (RT-qPCR), western blotting and immunohistochemistry. The correlation between CC10 and TFF1 expression was further analyzed using Spearman's correlation analysis. The expression of TFF1 was significantly increased in the sinus mucosa of patients with CRS and NP, whereas CC10 expression was significantly decreased compared with controls. Spearman's correlation analysis identified a negative correlation between CC10 and TFF1 expression in the sinus mucosa of patients with CRS and NP. The results of immunohistochemistry and RT-qPCR were consistent with each other. Hematoxylin and eosin staining revealed notable lesions in the mucous membranes, goblet cells and cilia of sinus mucosa samples from patients with CRS and NP. The negative correlation between CC10 and TFF1 expression during the progression of CRS and NP suggest that CC10 and TFF1 may serve important roles in its pathogenesis.

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Section: Discussionmentioning

confidence: 99%

“…CC10 is constitutively expressed in the epithelial cells of organs that directly communicate with the external environment, including the nose, bronchi and lungs (7)(8)(9). Furthermore, CC10 is an important mediator of inflammatory and allergic responses, as well as responses to malignant tumors of the respiratory system (10).…”

Section: Introductionmentioning

confidence: 99%

Expression of Clara cell 10-kDa protein and trefoil factor family 1 in patients with chronic rhinosinusitis and nasal polyps

Wang

2018

Exp Ther Med

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“…11 Global transcriptional profiling using oligonucleotide microarrays 12 provides a powerful tool to elucidate novel disease-related genes and pathways within complex tissues. 13 Because instillation of IL-13 to the lung recapitulates the asthma phenotype and administration of an IL-13 antagonist blocks OVA-challenge induced lung pathology, we investigated the expression profiles associated with disease induction and therapeutic intervention. The majority of pulmonary gene expression changes associated with the OVA-mediated response, with the exception of immunoglobulins, were also induced by IL-13 instillation.…”

Section: Introductionmentioning

confidence: 99%

Gene expression analysis in a murine model of allergic asthma reveals overlapping disease and therapy dependent pathways in the lung

Follettie¹,

Ellis²,

Donaldson

et al. 2006

Pharmacogenomics J

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Accumulating evidence in animal models and human asthma support a central role for IL-13 signaling in disease pathogenesis. In order to identify asthma and therapy associated genes, global transcriptional changes were monitored in mouse lung following antigen challenge (ovalbumin (OVA)), either alone or in the presence of a soluble IL-13 antagonist. Changes in whole lung gene expression after instillation of mIL-13 were also measured both in wild type and STAT6 deficient mice. A striking overlap in the gene expression profiles induced by either OVA challenge or mIL-13 was observed, further strengthening the relationship of IL-13 signaling to asthma. Consistent with results from functional studies, a subset of the OVA-induced gene expression was significantly inhibited by a soluble IL-13 antagonist while IL-13-modulated gene expression was completely attenuated in the absence of STAT6-mediated signaling. Results from these experiments greatly expand our understanding of asthma and provide novel molecular targets for therapy and potential biomarkers of IL-13 antagonism.

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“…Genetic susceptibility, infection, anatomic abnormalities and local immunologic imbalances have been postulated to play a role in its pathogenesis (11). Although numerous studies have recently dealt with the pathogenesis of this nasal disease, the molecular alterations required for its development and progression have yet to be well understood (12).…”

Section: Discussionmentioning

confidence: 99%

Gene expression analysis reveals novel altered genes in nasal polyps

Babeto

Calmon²,

Provazzi³

et al. 2010

Mol Med Rep

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Abstract. Nasal polyposis (NP) is a chronic inflammatory disease of the nasal mucosa characterized by the infiltration of inflammatory cells, mainly eosinophils. Although nasal polyposis occurs in 4% of the population, its physiopathology remains unclear. The aim of this study was to identify and characterize differentially expressed genes that can be used in the prognosis, treatment and elucidation of this physiopathology. To identify novel genes differentially expressed in NP, we applied real-time quantitative PCR to 11 NP samples and to a pool of total RNA from a subset of 13 normal nasal mucosa samples from human autopsies. For selecting genes, the methylated CpG island amplification technique was used. Five differentially methylated clones (ATP2A1, NOVA1, PLCD3, SOLH and TGFβI) were identified. However, these genes presented methylated CpG islands between exons, i.e., not in the promoter regions of the genes. Thus, as shown by real-time PCR, the ATP2A1, SOLH, PLDC3 and TGFβI genes were overexpressed in NP. The genes identified in this study are probably involved in some stage of the process of formation and development of nasal polyposis, as they were highly expressed in the nasal polyp samples.

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Gene expression profiles in human nasal polyp tissues studied by means of DNA microarray

Cited by 109 publications

References 40 publications

Expression of Clara cell 10-kDa protein and trefoil factor family 1 in patients with chronic rhinosinusitis and nasal polyps

Expression of Clara cell 10-kDa protein and trefoil factor family 1 in patients with chronic rhinosinusitis and nasal polyps

Gene expression analysis in a murine model of allergic asthma reveals overlapping disease and therapy dependent pathways in the lung

Gene expression analysis reveals novel altered genes in nasal polyps

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