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Alterations in alveolar epithelium differentiation and vasculogenesis in lungs of LIF/IGF‐I double deficient embryos
Author(s) -
MorenoBarriuso Nuria,
LópezMalpartida Ana V.,
de Pablo Flora,
Pichel José G.
Publication year - 2006
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.20842
Subject(s) - leukemia inhibitory factor , biology , lung , mesenchyme , respiratory epithelium , vasculogenesis , alveolar epithelium , epithelium , embryo , respiratory system , alveolar cells , endocrinology , andrology , pathology , medicine , microbiology and biotechnology , immunology , anatomy , stem cell , progenitor cell , inflammation , interleukin 6 , genetics
Abstract Previous studies on double deficient mice for leukemia inhibitory factor (LIF) and insulin‐like growth factor I (IGF‐I) reported that they died of respiratory failure, with abnormal lung histology and altered expression of pulmonary markers. Here we analyzed prenatal Lif/Igf‐I double mutant mouse embryos to characterize LIF and IGF‐I cooperative roles in distal lung epithelium and vascular maturation. Lungs of IGF‐I‐deficient embryos displayed a higher proportion of type II pneumocytes, less differentiated type I pneumocytes, and failure in alveolar capillary remodeling compared to wild type and LIF‐deficient mice. Lif/Igf‐I double knockout lungs showed aggravated pulmonary hypoplasia, lower airway volume, increased proliferation, and elevated levels of ERK1/2 activation. In addition, their alveoli were collapsed and lined by type II cells. The differentiation of type I cells barely occurred and capillaries remained in the abundant mesenchyme. These results indicate that LIF collaborates with IGF‐I in lung alveolar epithelium and vascular maturation. Developmental Dynamics 235:2040–2050, 2006. © 2006 Wiley‐Liss, Inc.