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Glucocorticoids increase the fluidity of the fetal-rat liver microsomal membrane in the perinatal period.

ABSTRACT: Dexamethasone, a synthetic glucocorticoid, was administered to pregnant rats during the last week of pregnancy in order to examine its effects on the fluidity of the developing fetal-rat liver microsomal membrane. This early prenatal exposure to dexamethasone, which preceded the natural appearance of fetal corticosteroids, markedly accelerated the normal perinatal course of fluidization of this membrane. The lipid apparent microviscosity, which was determined by measurement of fluorescence polarization, decreased in 21-days-old treated fetuses to values that were indistinguishable from those of untreated newborn rats. This dexamethasone-mediated acceleration of membrane fluidization was associated with an increase in the index of unsaturation of the fatty acyl moiety of microsomal lipids. Dexamethasone caused a significant increase in the microsomal content of polyunsaturated fatty acids (arachidonic and linoleic acid), which was accompanied by a decrease in content of monoenoic fatty acids (oleic and palmitoleic acid). This early exposure in utero to dexamethasone precociously induced the changes in fatty acid composition of fetal-rat liver microsomal lipids that normally occur between the last day of pregnancy and the first day of extra-uterine life. These results suggest that endogenous glucocorticoids play a major role in the perinatal fluidization of the rat liver microsomal membrane.

SUBMITTER: Kapitulnik J

PROVIDER: S-EPMC1147236 | biostudies-other | 1986 Oct

REPOSITORIES: biostudies-other

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Project description:Endothelial cells (ECs) lining the blood vessels serve a variety of functions and play a central role in the homeostasis of the circulatory system. Since the ductus arteriosus (DA) has different arterial characteristics from its connecting vessels, we hypothesized that ECs of the DA exhibited a unique gene profile involved in the regulation of DA-specific morphology and function. Using a fluorescence-activated cell sorter, we isolated ECs from pooled tissues from the DA or the descending aorta of Wistar rat fetuses at full-term of gestation (F group) or neonates 30 minutes after birth (N group). Using anti-CD31 and anti-CD45 antibodies as cell surface markers for ECs and hematopoietic derived cells, respectively, cDNAs from the CD31-positive and CD45-negative cells were hybridized to the Affymetrix GeneChip® Rat Gene 1.0 ST Array. Among 26,469 gene-level probe sets, 82 genes in the F group and 81 genes in the N group were expressed at higher levels in DA ECs than in aortic ECs (p<0.05, fold change>2.0). In addition to well-known endothelium-enriched genes such as Tgfb2 and Vegfa, novel DA endothelium-dominant genes including Slc38a1, Capn6, and Lrat were discovered. Enrichment analysis using GeneGo MetaCore software showed that DA endothelium-related biological processes were involved in morphogenesis and development. We identified many overlapping genes in each process including neural crest-related genes (Hoxa1, Hoxa4, and Hand2, etc) and the second heart field-related genes (Tbx1, Isl1, and Fgf10, etc). Moreover, we found that regulation of epithelial-to-mesenchymal transition, cell adhesion, and retinol metabolism are the active pathways involved in the network via potential interactions with many of the identified genes to form DA-specific endothelia. In conclusion, the present study uncovered several significant differences of the transcriptional profile between the DA and aortic ECs. Newly identified DA endothelium-dominant genes may play an important role in DA-specific functional and morphologic characteristics.

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Glucocorticoids increase the fluidity of the fetal-rat liver microsomal membrane in the perinatal period.

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