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This Article Full Text Full Text (PDF) All Versions of this Article: JOE-08-0238v1 JOE-08-0238v2 200/3/321    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Provost, P. R Articles by Tremblay, Y. Search for Related Content PubMed PubMed Citation Articles by Provost, P. R Articles by Tremblay, Y.

¹ Laboratory of Ontogeny and Reproduction, Rm T-2-67, Centre Hospitalier Universitaire de Québec, Pavillon CHUL, 2705 Laurier Boulevard, Québec City, Québec, Canada G1V 4G2² Department of Obstetrics and Gynecology, Faculty of Medicine, Laval University, Québec City, Québec, Canada G1V 4G2³ Centre de Recherche en Biologie de la Reproduction (CRBR), Laval University, Québec City, Québec, Canada G1V 4G2

(Correspondence should be addressed to Y Tremblay; Email: yves.tremblay{at}crchul.ulaval.ca)

*(P R Provost and E Boucher contribute equally to this work)

A sex difference in surfactant lipids is associated with a higher incidence of respiratory distress syndrome for males in cases of preterm birth. In animal models, the sex difference in surfactant lipids was shown to be androgen receptor-dependent. This report examines expression of apolipoprotein (apo)A-I, apoA-II, apoC-II, apoE, apoH, and lipoprotein lipase (LPL) by quantitative real-time PCR in pools of male and female fetal lung tissues from various mouse litters from gestation day (GD) 15.5 to 18.5, and in various adult tissues. Although the expression profiles of ApoA-I, ApoA-II, ApoC-II, and ApoH are complex, these genes are co-regulated and they all present a sex difference (P=0.0896, 0.0896, 0.0195, and 0.0607 respectively) with higher expression for females for several litters. Pulmonary expression of apoA-I, apoA-II, and apoH were specific to the developing lung. ApoE and LPL mRNAs showed a significant increase from GD 17.5 to 18.5. An increase in apoA-I-, apoA-II-, apoC-II-, and apoH-mRNA accumulation was observed from GD 16.5 to 17.5 in correlation with the emergence of mature type II pneumonocytes. These four apolipoprotein genes are co-regulated with type 2 and 5 17β-hydroxysteroid dehydrogenases, which are respectively involved in inactivation and synthesis of androgens. Finally, apoC-II was detected by immunohistochemistry in epithelial cells of the distal epithelium. Positive signals looking like secretory granules were located near the basal membrane. Our results are compatible with a role for apolipoproteins in lipid metabolism and transport in the developing lung in association with the sex difference in surfactant lipid synthesis.