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1: J Cell Biochem. 2007 Apr 15;100(6):1415-29.

Key developmental regulators change during hyperoxia-induced injury and recovery 
in adult mouse lung.

Pogach MS, Cao Y, Millien G, Ramirez MI, Williams MC.

Pulmonary Center, Boston University, Boston, Massachusetts 02118, USA.
[e-mail]

Developmentally important genes have recently been linked to tissue regeneration 
and epithelial cell repair in neonatal and adult animals in several organs,
including liver, skin, prostate, and musculature. We hypothesized that
developmentally important genes play roles in lung injury repair in adult mice.
Although there is considerable information known about these processes, the
specific molecular pathways that mediate injury and regulate tissue repair are
not fully elucidated. Using a hyperoxic injury model to study these mechanisms of
lung injury and tissue repair, we selected the following genes based upon their
known or putative roles in lung development and organogenesis: TTF-1, FGF9,
FGF10, BMP4, PDGF-A, VEGF, Ptc, Shh, Sca-1, BCRP, CD45, and Cyclin-D2. Our
findings demonstrate that several developmentally important genes (Sca-1, Shh,
PDGF-A, VEGF, BCRP, CD45, BMP4, and Cyclin-D2) change during hyperoxic injury and
normoxic recovery in mice, suggesting that adult lung may reactivate key
developmental regulatory pathways for tissue repair. The mRNA for one gene
(TTF-1), unchanged during hyperoxia, was upregulated late in recovery phase.
These novel findings provide the basis for testing the efficacy of post-injury
lung repair in animals genetically modified to inactivate or express individual
molecules.

PMID: 17167788 [PubMed - indexed for MEDLINE]

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