Pulmonary development in the fetal one-humped camel: morphometry

Sayed, Ramy K. A.; Atoji, Yasuro; Kamel, Gamal; Moneim, Mohamed A.; Yamamoto, Yoshio; Suzuki, Yoshitake

doi:10.1016/s0940-9602(98)80070-8

Cited by 1 publication

(1 citation statement)

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“…Early-stage fetal lungs can develop in serumless, chemically defined medium with normal spatial and temporal patterns in vitro [ 17 , 22 ], and the cultured embryonic lung is widely used to identify regulators of lung development. In previous in vivo studies, fetal lung saccular circumference and area per unit increased as pregnancy progressed [ 37 ], and the fetal rat lung at E15.5 is in a pseudoglandular period, with epithelial cells progressively differentiating from a columnar epithelium to a cuboidal epithelium [ 2 ]. We observed that fetal lung development under control conditions in vitro was similar to that in vivo .…”

Section: Discussionmentioning

confidence: 99%

N-Methyl-D-aspartate Receptor Excessive Activation Inhibited Fetal Rat Lung DevelopmentIn VivoandIn Vitro

Liao

Zhou

Luo

et al. 2016

BioMed Research International

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Background. Intrauterine hypoxia is a common cause of fetal growth and lung development restriction. Although N-methyl-D-aspartate receptors (NMDARs) are distributed in the postnatal lung and play a role in lung injury, little is known about NMDAR's expression and role in fetal lung development. Methods. Real-time PCR and western blotting analysis were performed to detect NMDARs between embryonic days (E) 15.5 and E21.5 in fetal rat lungs. NMDAR antagonist MK-801's influence on intrauterine hypoxia-induced retardation of fetal lung development was tested in vivo, and NMDA's direct effect on fetal lung development was observed using fetal lung organ culture in vitro. Results. All seven NMDARs are expressed in fetal rat lungs. Intrauterine hypoxia upregulated NMDARs expression in fetal lungs and decreased fetal body weight, lung weight, lung-weight-to-body-weight ratio, and radial alveolar count, whereas MK-801 alleviated this damage in vivo. In vitro experiments showed that NMDA decreased saccular circumference and area per unit and downregulated thyroid transcription factor-1 and surfactant protein-C mRNA expression. Conclusions. The excessive activation of NMDARs contributed to hypoxia-induced fetal lung development retardation and appropriate blockade of NMDAR might be a novel therapeutic strategy for minimizing the negative outcomes of prenatal hypoxia on lung development.

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