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SHR Neuro Cancer Cardio Lipid Metab Microb
Friedmacher, F; Gosemann, JH; Fujiwara, N; Takahashi, H; Hofmann, A; Puri, P.
Expression of Sproutys and SPREDs is decreased during lung branching morphogenesis in nitrofen-induced pulmonary hypoplasia.
Pediatr Surg Int. 2013; 29(11): 1193-1198.
Doi: 10.1007/s00383-013-3385-6
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PubMed
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- Leading authors Med Uni Graz
- Friedmacher Florian
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- Abstract:
- Pulmonary hypoplasia (PH) is a life-threatening condition associated with congenital diaphragmatic hernia (CDH), characterized by defective lung development. Sproutys and Sprouty-related proteins (SPREDs) play a key role in lung branching morphogenesis through modification of epithelial-mesenchymal interactions. During the pseudoglandular stage, Sproutys are highly expressed in distal airway epithelium, while SPREDs within the surrounding mesenchyme. Sprouty2/4 knockouts show severe defects in branching morphogenesis with reduced number of distal airways. SPRED-1 and SPRED-2 are strongly expressed in regions of new airway formation, highlighting their important function in branching pattern. We hypothesized that expression of Sprouty2, Sprouty4, SPRED-1 and SPRED-2 is decreased during lung branching morphogenesis in nitrofen-induced PH. Timed-pregnant rats received either nitrofen or vehicle on E9.5. On E15.5 (n = 16), fetal lungs were micro-dissected and divided into controls and PH, while on E18.5 (n = 24) groups were: control, PH without CDH [CDH(-)], and PH with CDH [CDH(+)]. Pulmonary gene expression levels of Sprouty2, Sprouty4, SPRED-1 and SPRED-2 were analyzed by qRT-PCR. Immunohistochemistry was performed to evaluate protein expression/distribution. On E18.5, relative mRNA expression levels of Sprouty2, Sprouty4, SPRED-1 and SPRED-2 were significantly decreased in CDH(-) and CDH(+) groups compared to controls (P < 0.05). Immunoreactivity of Sprouty2, Sprouty4, SPRED-1 and SPRED-2 was markedly diminished on E18.5 in nitrofen-induced PH. Decreased expression of Sproutys and SPREDs during the terminal pseudoglandular stage may disrupt lung branching morphogenesis by interfering with epithelial-mesenchymal interactions contributing to PH.
- Find related publications in this database (using NLM MeSH Indexing)
- Abnormalities, Multiple - chemically induced Abnormalities, Multiple - genetics Abnormalities, Multiple - metabolism
- Animals -
- Disease Models, Animal -
- Female -
- Fibroblast Growth Factors - antagonists & inhibitors
- Gene Expression Regulation, Developmental -
- Immunohistochemistry -
- Lung - abnormalities Lung - embryology Lung - metabolism
- Lung Diseases - chemically induced Lung Diseases - genetics Lung Diseases - metabolism
- MAP Kinase Signaling System -
- Morphogenesis - genetics
- Nerve Tissue Proteins - biosynthesis Nerve Tissue Proteins - genetics
- Phenyl Ethers - toxicity
- Pregnancy -
- Pregnancy, Animal -
- RNA, Messenger - genetics
- Rats -
- Rats, Sprague-Dawley -
- Real-Time Polymerase Chain Reaction -
- Repressor Proteins - biosynthesis Repressor Proteins - genetics
- Reverse Transcriptase Polymerase Chain Reaction -
- Find related publications in this database (Keywords)
- Sprouty
- SPRED
- Lung development
- Pulmonary hypoplasia
- Congenital diaphragmatic hernia
- Nitrofen