ArticleRespiratory research2012
Endothelial-monocyte activating polypeptide II disrupts alveolar epithelial type II to type I cell transdifferentiation.
Article in Respiratory research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Ambroxol for women at risk of preterm birth for preventing neonatal respiratory distress syndrome.The Cochrane database of systematic reviews · 2014Pooled it
- [Research progress on the cellular and molecular mechanisms of tooth eruption].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2016Article
- Adapted approach to profile genes while reconciling Vegf-a mRNA expression in the developing and injured lung.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Vascular mediators in chronic lung disease of infancy: role of endothelial monocyte activating polypeptide II (EMAP II).Birth defects research. Part A, Clinical and molecular teratology · 2014Review
- Ephrin-B2 reverse signaling increases α5β1 integrin-mediated fibronectin deposition and reduces distal lung compliance.American journal of respiratory cell and molecular biology · 2013Article
- Cell proliferation and migration are modulated by Cdk-1-phosphorylated endothelial-monocyte activating polypeptide II.PloS one · 2012Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundDistal alveolar morphogenesis is marked by differentiation of alveolar type (AT)-II to AT-I cells that give rise to the primary site of gas exchange, the alveolar/vascular interface. Endothelial-Monocyte Activating Polypeptide (EMAP) II, an endogenous protein with anti-angiogenic properties, profoundly disrupts distal lung neovascularization and alveolar formation during lung morphogenesis, and is robustly expressed in the dysplastic alveolar regions of infants with Bronchopulmonary dysplasia. Determination as to whether EMAP II has a direct or indirect affect on ATII → ATI trans-differentiation has not been explored.
methodIn a controlled nonvascular environment, an in vitro model of ATII → ATI cell trans-differentiation was utilized to demonstrate the contribution that one vascular mediator has on distal epithelial cell differentiation.
resultsHere, we show that EMAP II significantly blocked ATII → ATI cell transdifferentiation by increasing cellular apoptosis and inhibiting expression of ATI markers. Moreover, EMAP II-treated ATII cells displayed myofibroblast characteristics, including elevated cellular proliferation, increased actin cytoskeleton stress fibers and Rho-GTPase activity, and increased nuclear:cytoplasmic volume. However, EMAP II-treated cells did not express the myofibroblast markers desmin or αSMA.
conclusionOur findings demonstrate that EMAP II interferes with ATII → ATI transdifferentiation resulting in a proliferating non-myofibroblast cell. These data identify the transdifferentiating alveolar cell as a possible target for EMAP II's induction of alveolar dysplasia.
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