Embigin deficiency leads to delayed embryonic lung development and high neonatal mortality in mice
Embigin (Gp70), a receptor for fibronectin and an ancillary protein for monocarboxylate transporters, is known to regulate stem cell niches in sebaceous gland and bone marrow. Here, we show that embigin expression is at high level during early mouse embryogenesis and that embigin is essential for lung development. Markedly increased neonatal mortality of Emb-/- mice can be explained by the compromised lung maturation: in Emb-/- mice (E17.5) the number and the size of the small airways and distal airspace are significantly smaller, there are fewer ATI and ATII cells, and the alkaline phosphatase activity in amniotic fluid is lower. Emb-/- lungs show less peripheral branching already at E12.5, and embigin is highly expressed in lung primordium. Thus, embigin function is essential at early pseudoglandular stage or even earlier. Furthermore, our RNA-seq analysis and Ki67 staining results support the idea that the development of Emb-/- lungs is rather delayed than defected.
Published on December 10, 2024
ABSTRACT
PMID:38318368 | PMC:PMC10839689 | DOI:10.1016/j.isci.2024.108914
Turku Bioscience Centre[Affiliation]
Back to PublicationsLatest Publications
- Author response to “Commentary on detoxification of deoxynivalenol by pathogen-inducible tau-class glutathione transferases from wheat” by Dr. Latika Shendre
- Editorial: Epigenetic regulation of T cell function in type 1 diabetes
- Prenatal exposure to persistent organic pollutants modulates the metabolism and gut microbiota of the offspring
- Preventing Proteomics Data Tombs Through Collective Responsibility and Community Engagement
- Cell viscosity influences haematogenous dissemination and metastatic extravasation of tumour cells