|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Cardiovascular Research Institute and Departments of Pediatrics and Surgery, University of California San Francisco, San Francisco, California, USA
* To whom correspondence should be addressed. E-mail: cheri{at}itsa.ucsf.edu.
Fetal tracheal occlusion (TO) has been reported to stimulate lung growth but decreases number and maturation of type II cells, effects that vary with gestational age and duration of TO. We examined effects of a novel method of TO (unipolar microcautery to seal the trachea) produced at 19.5-20d gestation in fetal rats; fetuses were delivered at term, 22d. Controls were sham operated and unoperated littermates. TO increased wet lung weight, but not dry lung weight or lung DNA and protein. To evaluate further the effects of TO, we examined the cell cycle regulators, cyclins D1 and A, in fetal lungs. Cyclin D1 increased with TO (P<0.005). TO also increased expression of the type I epithelial cell marker, RTI40 (mRNA and protein). TO decreased mRNA for surfactant proteins (SP) -A and -C but did not affect protein levels of SP-A and -B and of RTII70, a type II epithelial cell marker. We conclude that TO by microcautery, even of short duration, has diverse pulmonary effects including stimulating increased levels of cyclin D1 with probable cell cycle progression, type I cell differentiation and possibly inhibiting type II cell function.
This article has been cited by other articles:
![]() |
C. J. Chapin, R. Ertsey, J. Yoshizawa, A. Hara, L. Sbragia, J. J. Greer, and J. A. Kitterman Congenital diaphragmatic hernia, tracheal occlusion, thyroid transcription factor-1, and fetal pulmonary epithelial maturation Am J Physiol Lung Cell Mol Physiol, July 1, 2005; 289(1): L44 - L52. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |