Publication: Microarray analysis of Myf5-/-:MyoD-/- hypoplastic mouse lungs reveals a profile of genes involved in pneumocyte differentiation
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Date
2007
Authors
Baguma-Nibasheka, M. ; Angka, H.E. ; Inanlou, M.R. ; Kablar, B.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Fetal breathing-like movements (FBMs) are
important in normal lung growth and pneumocyte
differentiation. In amyogenic mouse embryos
(designated as Myf5-/-:MyoD-/-, entirely lacking skeletal
musculature and FBMs), type II pneumocytes fail to
differentiate into type I pneumocytes, the cells
responsible for gas exchange, and the fetuses die from
asphyxia at birth. Using oligonucleotide microarrays, we
compared gene expression in the lungs of Myf5-/-
:MyoD-/- embryos to that in normal lungs at term. Nine
genes were found to be up-regulated and 54 downregulated
at least 2-fold in the lungs of double-mutant
embryos. Since many down-regulated genes are
involved in lymphocyte function, immunohistochemistry
was employed to study T- and B-cell maturity in the
thymus and spleen. Our findings of normal lymphocyte
maturity implied that the down-regulation was specific
to the double-mutant lung phenotype and not to its
immune system. Immunostaining also revealed altered
distribution of transcription and growth factors (SATB1,
c-Myb, CTGF) from down-regulated genes whose
knockouts are now known to undergo embryonic or
neonatal death secondary to respiratory failure. Together,
it appears that microarray analysis has identified a
profile of genes potentially involved in pneumocyte
differentiation and therefore in the mechanisms that may
be implicated in the mechanochemical signal
transduction pathways underlying FBMs-dependent pulmonary hypoplasia.
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