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An Experimental System to Study Mechanotransduction in Fetal Lung Cells
Published on: February 16, 2012
HDL and vitamin E in plasma and the expression of SR-BI on lung cells during rat perinatal development
1Department of Neonatology, University Hospital Charité, Humboldt University, 10098 Berlin, Germany.
Insights
Neonates have low vitamin E levels, increasing oxidative injury risk. Vitamin E uptake by lung cells develops around birth, crucial for timing supplementation to protect preterm infants from lung damage.
Area of Science:
- Biochemistry
- Neonatal Physiology
- Antioxidant Research
Background:
- Vitamin E is a key lipophilic antioxidant crucial for preventing oxidant-caused injuries.
- Neonates are particularly vulnerable to oxidative stress due to low vitamin E concentrations.
- Optimal vitamin E supplementation timing, form, and dosage for neonates remain undetermined.
Purpose of the Study:
- To investigate the developmental pattern of vitamin E uptake by alveolar type II cells in fetal and neonatal rats.
- To correlate vitamin E plasma levels and scavenger receptor class B type I (SR-BI) expression with cellular uptake capacity.
- To inform the optimal timing for vitamin E supplementation in preterm neonates to prevent oxidative lung injury.
Main Methods:
- Measurement of plasma vitamin E, cholesterol, and fatty acid ratios during rat fetal development.
- Assessment of scavenger receptor class B type I (SR-BI) expression on fetal and neonatal lung cells.
- Correlation analysis between plasma lipid profiles and SR-BI expression patterns.
Main Results:
- Plasma vitamin E, HDL cholesterol, and vitamin E/fatty acid ratios decreased during late fetal development, reaching a minimum before birth.
- SR-BI expression was undetectable in fetal lung cells until the perinatal period, mirroring plasma lipid changes.
- These parameters increased postnatally, approaching adult levels.
Conclusions:
- Alveolar type II cell capacity for vitamin E uptake develops perinatally in mature neonates.
- The developmental timing of SR-BI expression and plasma vitamin E availability is critical for cellular vitamin E supply.
- Consideration of this developmental window is essential for establishing effective vitamin E supplementation strategies for preterm infants.
Abstract:
Vitamin E is the most important lipophilic antioxidant, and beneficial effects on oxidant-caused injuries have been reported. Neonates are at high risk of oxidative injury in the lung and other organs because of a low vitamin E concentration, but the optimal timing of the application, a safe application form, and the optimal dosage of vitamin E are not known at present. We recently showed that alveolar type II cells take up vitamin E preferentially from high-density lipoprotein (HDL), probably by means of the candidate HDL receptor, scavenger receptor class B type I (SR-BI; Kolleck et al. Free Rad Biol Med 27; 882-890, 1999). Therefore, both the HDL-bound vitamin E in plasma and the expression of SR-BI on alveolar type II cells may determine the supply of the cells with vitamin E. We show here that the plasma level of vitamin E, total and HDL cholesterol, and the ratio of vitamin E to polyunsaturated fatty acids and to total fatty acids decrease during fetal rat development, reaching the minimum at the postconceptual day 21 (day -1). These parameters increase thereafter to about the same levels as in adult rats. SR-BI is not detectable until day -1 on fetal lung cells, but the expression during the postnatal phase follows the same pattern as the plasma lipid constituents. We conclude that the ability of alveolar type II cells to take up vitamin E develops perinatally in mature neonates. This aspect also has to be considered when the optimal timing of supplementation for the protection of preterm neonates with vitamin E against oxidative lung injury is established.
