ArticleBirth defects research. Part A, Clinical and molecular teratology2008
Unique spatial and cellular expression patterns of Hoxa5, Hoxb4, and Hoxb6 proteins in normal developing murine lung are modified in pulmonary hypoplasia.
Article in Birth defects research. Part A, Clinical and molecular teratology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Cancer gene mutations in congenital pulmonary airway malformation patients.ERJ open research · 2019Article
- HOXA5 and p53 cooperate to suppress lung cancer cell invasion and serve as good prognostic factors in non-small cell lung cancer.Journal of Cancer · 2017Article
- Article
- Oxygen differentially affects the hox proteins Hoxb5 and Hoxa5 altering airway branching and lung vascular formation.Journal of cell communication and signaling · 2014Article
- A new scenario of the evolutionary derivation of the mammalian diaphragm from shoulder muscles.Journal of anatomy · 2013Article
- Regulatory interactions between androgens, Hoxb5, and TGF β signaling in murine lung development.BioMed research international · 2013Article
- Article
- Congenital diaphragmatic hernia candidate genes derived from embryonic transcriptomes.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- c-Kit is essential for alveolar maintenance and protection from emphysema-like disease in mice.American journal of respiratory and critical care medicine · 2011Article
- Presenilin-1 processing of ErbB4 in fetal type II cells is necessary for control of fetal lung maturation.Biochimica et biophysica acta · 2011Article
- Aberrant cell adhesion molecule expression in human bronchopulmonary sequestration and congenital cystic adenomatoid malformation.American journal of physiology. Lung cellular and molecular physiology · 2009Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundHox transcription factors modulate signaling pathways controlling organ morphogenesis and maintain cell fate and differentiation in adults. Retinoid signaling, key in regulating Hox expression, is altered in pulmonary hypoplasia. Information on pattern-specific expression of Hox proteins in normal lung development and in pulmonary hypoplasia is minimal. Our objective was to determine how pulmonary hypoplasia alters temporal, spatial, and cellular expression of Hoxa5, Hoxb4, and Hoxb6 proteins compared to normal lung development.
methodsTemporal, spatial, and cellular Hoxa5, Hoxb4, and Hoxb6 expression was studied in normal (untreated) and nitrofen-induced hypoplastic (NT-PH) lungs from gestational day 13.5, 16, and 19 fetuses and neonates using Western blot and immunohistochemistry.
resultsModification of protein levels and spatial and cellular Hox expression patterns in NT-PH lungs was consistent with delayed lung development. Distinct protein isoforms were detected for each Hox protein. Expression levels of the Hoxa5 and Hoxb6 protein isoforms changed with development and were altered further in NT-PH lungs. Compared to normal lungs, GD19 and neonatal NT-PH lungs had decreased Hoxb6 and increased Hoxa5 and Hoxb4. Hoxa5 cellular localization changed from mesenchyme to epithelia earlier in normal lungs. Hoxb4 was expressed in mesenchyme and epithelial cells throughout development. Hoxb6 remained mainly in mesenchymal cells around distal airways.
conclusionsUnique spatial and cellular expression of Hoxa5, Hoxb4, and Hoxb6 participates in branching morphogenesis and terminal sac formation. Altered Hox protein temporal and cellular balance of expression either contributes to pulmonary hypoplasia or functions as a compensatory mechanism attempting to correct abnormal lung development and maturation in this condition.
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