Ontogeny of Surfactant Apoproteins in the Rat

Schellhase, Dennis E.; Emrie, Philip A.; Fisher, James H.; Shannon, John M.

doi:10.1203/00006450-198909000-00001

Cited by 95 publications

(57 citation statements)

References 23 publications

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“…Whatever the mechanism, our data indicate that each of the SPs are differentially regulated after birth and can be regulated independently of AEC differentiation. This finding is consistent with previous studies demonstrating that each of the SPs can have a different pattern of expression following birth (12,(22)(23)(24). Numerous transcription factors have been implicated in regulating SP expression (25,26), and, therefore, it is possible that the differential SP gene expression is related to differences in their function (27,28).…”

supporting

confidence: 82%

Alveolar Epithelial Cell Differentiation and Surfactant Protein Expression After Mild Preterm Birth in Sheep

et al. 2006

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ABSTRACT:As the transition to extrauterine life at birth alters the proportions of type I and II alveolar epithelial cells (AECs), our aim was to determine the effect of mild preterm birth on AECs and surfactant protein (SP) gene expression. Preterm lambs were born at ϳ133 d of gestational age (DGA); controls were born at term (ϳ147 DGA). Lungs were collected from preterm lambs at termequivalent age (TEA; ϳ2 wk after preterm birth) and 6 wk post-TEA. Control lung tissue was collected from fetuses (at 132 DGA), as well as from lambs at ϳ6 h (normal term) and 2, 6, and 8 wk of postnatal age (PNA). In controls, the proportion of type I AECs decreased from 65.1 Ϯ 3.9% at term to 50.9 Ϯ 3.3%, while the proportion of type II AECs increased from 33.7 Ϯ 3.9% to 48.5 Ϯ 3.3% at 6 wk PNA. At 2 wk after preterm birth, the proportions of type I and II AECs were similar in preterm lambs compared to 132-d fetal levels and term controls but differed from control values at 2 wk PNA; differences between control and preterm lambs persisted at 8 wk PNA. At ϳ2 wk after preterm birth, SP-A and SP-B, but not SP-C, mRNA levels were significantly reduced in preterm lambs compared with term controls, but these differences did not persist at 2 and 6 wk PNA. We conclude that mild preterm birth alters the normal postnatal changes in type I and II cell proportions but does not severely affect SP gene expression.

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confidence: 82%

Alveolar Epithelial Cell Differentiation and Surfactant Protein Expression After Mild Preterm Birth in Sheep

et al. 2006

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“…Although lung surfactant contains predominantly phospholipids, a class of lipids absent from barrier lipids, both secretory systems deliver lipid to their respective extracellular domains (1)(2)(3)(12)(13)(14). Moreover, the epidermal and lung lamellar secretory systems exhibit striking similarities in their developmental timetables, with both maturing in the third trimester in humans and other animals (4,(8)(9)(10)(11)15). In the fetal rat, lamellar bodies first appear in skin and lung on gestational d 18; secretion begins on d 19 and 20, respectively; and maturation of both tissue systems is complete by d 21 of gestation (normal parturition occurs on d 22) (15,16).…”

Section: Introductionmentioning

confidence: 99%

“…The development of an analogous lamellar body secretory system in the type II alveolar cell pneumocyte has been studied widely in humans and in experimental animals (8)(9)(10)(11). Although lung surfactant contains predominantly phospholipids, a class of lipids absent from barrier lipids, both secretory systems deliver lipid to their respective extracellular domains (1)(2)(3)(12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

Hormonal basis for the gender difference in epidermal barrier formation in the fetal rat. Acceleration by estrogen and delay by testosterone.

Hanley

Rassner²,

Jiang³

et al. 1996

J. Clin. Invest.

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Previous studies have shown that ontogeny of the epidermal permeability barrier and lung occur in parallel in the fetal rat, and that pharmacologic agents, such as glucocorticoids and thyroid hormone, accelerate maturation at comparable developmental time points. Gender also influences lung maturation, i.e., males exhibit delayed development. Sex steroid hormones exert opposite effects on lung maturation, with estrogens accelerating and androgens inhibiting. In this study, we demonstrate that cutaneous barrier formation, measured as transepidermal water loss, is delayed in male fetal rats. Administration of estrogen to pregnant mothers accelerates fetal barrier development both morphologically and functionally. Competent barriers also form sooner in skin explants incubated in estrogen-supplemented media in vitro. In contrast, administration of dihydrotestosterone delays barrier formation both in vivo and in vitro.

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“…The mRNA levels of SP-D in rats also increase in response to glucocorticoid treatment, both in vitro and in vivo (32,33). Similarly, SP-A, SP-B, and SP-C mRNA levels also increase developmentally during fetal life (28,34,35). On the other hand, the levels of surfactant proteins (SP-A, SP-B) and the levels of SP mRNAs (SP-A, SP-B, SP-C) in rats are reduced (36,37) in fetuses of STZ-DB pregnancy.…”

mentioning

confidence: 89%

“…We tried to increase the intensity of the SP-B hybridization by using twice the number of nuclei and two labeled nucleotides. The failure to obtain a strong SP-B hybridization may in part be accounted for by delayed SP-B expression during development (34).…”

Section: Animal Model Diabetes Was Induced In Nonpregnant Femalementioning

confidence: 99%

Dexamethasone Enhances Surfactant Protein Gene Expression in Streptozotocin-Induced Immature Rat Lungs

1995

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Because surfactant protein (SP) mRNA levels in rat fetuses are increased by maternal dexamethasone (dex) treatment and decreased in streptozotocin-induced diabetic (STZ-DB) pregnancy, we investigated the in vivo effects of dex on SP gene expression in STZ-DB pregnancy. 2) a 2-3-fold increase in SP-C mRNA levels was observed in response to dex in d 18 and 20 fetuses; 3) the increase in transcription of SP-A and SP-B in d 20 fetuses after dex is 68 and 60%, respectively, of the increase in their mRNA levels whereas in STZ-DB, the decrease in transcription compared with mRNA levels is 3.67-fold for SP-A and 2.42 fold SP-B; and 4) changes in SP-C transcription in either in vivo model, dex-treated or STZ-DB, correspond well with changes in mRNA levels. Together, these findings indicate that dex can enhance SP expression in STZ-DB immature lungs and support differential regulation of fetal SP genes in the models studied. (Pediatr Res 38: 870-877, 1995)

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Ontogeny of Surfactant Apoproteins in the Rat

Cited by 95 publications

References 23 publications

Alveolar Epithelial Cell Differentiation and Surfactant Protein Expression After Mild Preterm Birth in Sheep

Alveolar Epithelial Cell Differentiation and Surfactant Protein Expression After Mild Preterm Birth in Sheep

Hormonal basis for the gender difference in epidermal barrier formation in the fetal rat. Acceleration by estrogen and delay by testosterone.

Dexamethasone Enhances Surfactant Protein Gene Expression in Streptozotocin-Induced Immature Rat Lungs

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