Variation in the bombesin staining of pulmonary neuroendocrine cells in pediatric pulmonary disorders—A useful marker for airway maturity

2020 ◽  
Vol 55 (9) ◽  
pp. 2383-2388
Author(s):  
Nagehan Emiralioğlu ◽  
Diclehan Orhan ◽  
Güzin Cinel ◽  
Gökçen Dilşa Tuğcu ◽  
Ebru Yalçın ◽  
...  
Keyword(s):  
Neuroendocrine Cells ◽  
Pulmonary Neuroendocrine Cells

Standardization of formaldehyde-induced fluorescence and its measurement to quantify serotonin emission in pulmonary neuroendocrine cells

1982 ◽  
Vol 75 (2) ◽  
pp. 251-258 ◽  
Author(s):  
I. M. Keith ◽  
L. A. Wiley ◽  
J. A. Will
Keyword(s):  
Neuroendocrine Cells ◽  
Pulmonary Neuroendocrine Cells

scholarly journals Cell-autonomous immune gene expression is repressed in pulmonary neuroendocrine cells and small cell lung cancer

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Ling Cai ◽  
Hongyu Liu ◽  
Fang Huang ◽  
Junya Fujimoto ◽  
Luc Girard ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Neuroendocrine Cells ◽  
Immune Gene ◽  
Small Cell Lung ◽  
Immune Gene Expression ◽  
Pulmonary Neuroendocrine Cells

AbstractSmall cell lung cancer (SCLC) is classified as a high-grade neuroendocrine (NE) tumor, but a subset of SCLC has been termed “variant” due to the loss of NE characteristics. In this study, we computed NE scores for patient-derived SCLC cell lines and xenografts, as well as human tumors. We aligned NE properties with transcription factor-defined molecular subtypes. Then we investigated the different immune phenotypes associated with high and low NE scores. We found repression of immune response genes as a shared feature between classic SCLC and pulmonary neuroendocrine cells of the healthy lung. With loss of NE fate, variant SCLC tumors regain cell-autonomous immune gene expression and exhibit higher tumor-immune interactions. Pan-cancer analysis revealed this NE lineage-specific immune phenotype in other cancers. Additionally, we observed MHC I re-expression in SCLC upon development of chemoresistance. These findings may help guide the design of treatment regimens in SCLC.

Maternal Smoking and Pulmonary Neuroendocrine Cells in Sudden Infant Death Syndrome

PEDIATRICS ◽  
1996 ◽  
Vol 98 (4) ◽  
pp. 668-672
Author(s):  
Ernest Cutz ◽  
Donald G. Perrin ◽  
Richard Hackman ◽  
Elinor N. Czegledy-Nagy
Keyword(s):  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Airway Epithelium ◽  
Maternal Smoking ◽  
Matched Control ◽  
Sudden Infant Death ◽  
Neuroendocrine Cells ◽  
Sudden Infant ◽  
Neuroepithelial Bodies ◽  
Pulmonary Neuroendocrine Cells

Background. Maternal smoking is a well-recognized risk factor for sudden infant death syndrome (SIDS), but the precise mechanism is unknown. We tested a hypothesis that maternal smoking affects pulmonary neuroendocrine cells (PNECs) and neuroepithelial bodies (NEBs), which are innervated PNEC clusters and presumed airway chemoreceptors. Methods. Lung sections from infants who died of SIDS and whose mothers smoked during pregnancy (n = 22), infants who died of SIDS and whose mothers were nonsmokers (n = 17), and age-matched control infants (n = 15) who died of other causes were immunostained for bombesin (a PNEC and NEB marker) and assessed morphometrically. Results. The frequency of PNEC (the percentage of airway epithelium immunoreactive for bombesin) was increased up to twofold in the lungs of infants who died of SIDS (7.7 ± 0.4%) compared with controls (4.9 ± 0.4%), as was the frequency (40 ± 3.5 vs 23 ± 3.7/cm2) and size (748 ± 46.5 vs 491 ± 25.8,µm2) of NEBs. In infants who died of SIDS and who were born to smoking mothers, PNEC frequency was increased significantly compared with that in those born to nonsmoking mothers, but the frequency and size of NEBs were not significantly different between the two groups. Conclusion. Our findings suggest that maternal smoking potentiates hyperplasia of the PNEC system in the lungs of infants who die of SIDS and that a dysfunction of these cells may contribute to the pathophysiology of SIDS.

Progesterone receptor isoform B expression in pulmonary neuroendocrine cells decreases cell proliferation

2019 ◽  
Vol 190 ◽  
pp. 212-223 ◽  
Author(s):  
Teeranut Asavasupreechar ◽  
Ryoko Saito ◽  
Dean P. Edwards ◽  
Hironobu Sasano ◽  
Viroj Boonyaratanakornkit
Keyword(s):  
Cell Proliferation ◽  
Progesterone Receptor ◽  
Neuroendocrine Cells ◽  
Pulmonary Neuroendocrine Cells ◽  
Isoform B

scholarly journals Efficient Generation and Transcriptomic Profiling of Human iPSC-Derived Pulmonary Neuroendocrine Cells

iScience ◽  
2020 ◽  
Vol 23 (5) ◽  
pp. 101083 ◽  
Author(s):  
Pooja Hor ◽  
Vasu Punj ◽  
Ben A. Calvert ◽  
Alessandra Castaldi ◽  
Alyssa J. Miller ◽  
...  
Keyword(s):  
Neuroendocrine Cells ◽  
Transcriptomic Profiling ◽  
Pulmonary Neuroendocrine Cells ◽  
Efficient Generation ◽  
Human Ipsc

scholarly journals The role of hypoxia and neurogenic genes (Mash-1 and Prox-1) in the developmental programming and maturation of pulmonary neuroendocrine cells in fetal mouse lung

2009 ◽  
Vol 90 (2) ◽  
pp. 180-195 ◽  
Author(s):  
Suzanne McGovern ◽  
Jie Pan ◽  
Guillermo Oliver ◽  
Ernest Cutz ◽  
Herman Yeger
Keyword(s):  
Developmental Programming ◽  
Neuroendocrine Cells ◽  
Mouse Lung ◽  
Fetal Mouse ◽  
Neurogenic Genes ◽  
Pulmonary Neuroendocrine Cells
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