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1 Inserm U492, Faculte de Medecine, Universite Paris XII, CRETEIL, France
* To whom correspondence should be addressed. E-mail: Jacques.Bourbon{at}creteil.inserm.fr.
Previous investigations gained from in vivo or lung explant studies suggested that VEGF is an autocrine proliferation and maturation factor for developing alveolar type II cells. The objective of this work was to determine whether VEGF exerted its growth and maturation effects directly on isolated type II cells. These were isolated from 19d-fetal rat lung and cultured in defined medium. The presence of VEGF receptor VEGFR2 was assessed in cultured cells at the pre- and post-translational levels. Recombinant VEGF165 formerly found to be active on lung explants failed to enhance type II cell proliferation estimated by thymidine and BrdU incorporation. It increased choline incorporation in saturated phosphatidylcholine by 27%, but did not increase phospholipid surfactant pool size. VEGF 100ng/ml let unchanged the transcript level of surfactant proteins SP-A, SP-C, and SP-D, but increased SP-B transcripts to 4 times the control steady-state level. VEGF slightly retarded, but did not prevent the in vitro transdifferentiation of type II into type I cells as assessed by immunolabeling of the type I cell marker T1
. We conclude that with the exception of SP-B
expression that appears to be controlled directly, the previously observed effects of this VEGF isoform upon type II cells are likely to be exerted indirectly through reciprocal paracrine interactions involving other lung cell types.
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