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in the newborn rat lung
1 The CIHR Group in Perinatal Research Centre, University of Alberta, Edmonton, Alberta, Canada
2 Department of Physiology, University of Alberta, Edmonton, Alberta, Canada; Department of Obstetrics and Gynaecology, University of Alberta, Edmonton, Alberta, Canada; Department of Pediatrics, University of Alberta, Edmonton, Alberta, Canada
* To whom correspondence should be addressed. E-mail: david.olson{at}ualberta.ca.
Signaling through the HIF-VEGF-VEGF receptor system (VEGF signaling system) leads to angiogenesis and epithelial cell proliferation and is a key mechanism regulating alveolarization in lungs of newborn rats. Hyperoxia exposure (>95% O2 day (d)4-14) arrests lung alveolarization and may do so through suppression of the VEGF signaling system. Lung tissue mRNA levels of HIF-2
and VEGF increased from d4-14 in normoxic animals, but hyperoxia suppressed these increases. Levels of HIF-2 and VEGF mRNA were highly correlated in both treatment groups suggesting that the oxygen-suppression of HIF-2 may be causal for decreased VEGF expression. VEGF164 protein levels increased with developmental age, and with hyperoxia to d9, but continuing hyperoxia decreased levels by d12. VEGFR1 and VEGFR2 mRNA expression also increased in air-exposed animals, and these too were significantly decreased by hyperoxia by d9 and d12, respectively. Receptor protein levels did not increase with development, however O2 did decrease protein to less than air values. Hyperoxic suppression of VEGF signaling from d9-14 may be one mechanism by which alveolarization is arrested.
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