Appearance of surfactant proteins, SP-A and SP-B, in developing rat lung and the effects of in vivo dexamethasone treatment

Shimizu, Hiroshi; Miyamura, Kazuo; Kuroki, Yoshio

doi:10.1016/0005-2760(91)90249-h

Cited by 47 publications

(37 citation statements)

References 32 publications

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“…In rabbits, it has been shown that corticosteroids (glucocorticoids) cause an increase in SP-B mRNA and a large increase in SP-A mRNA [48, 71, 84]. However, there is a difference between the two proteins in the magnitude of the response, indicating that the expression of SP-A and SP-B may be regulated independently [63,287]. It has been reported that the regulation of SP-A may be dependent on the dose and the time of exposure [140].…”

Section: Therapeutic Effects Of Hormonesmentioning

confidence: 99%

The Pulmonary Surfactant System: Biochemical and Clinical Aspects

Creuwels

Golde

Haagsman

1997

Lung

283

188

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Abstract. This article starts with a brief account of the history of research on pulmonary surfactant. We will then discuss the morphological aspects and composition of the pulmonary surfactant system. We describe the hydrophilic surfactant proteins A and D and the hydrophobic surfactant proteins B and C, with focus on the crucial roles of these proteins in the dynamics, metabolism, and functions of pulmonary surfactant. Next we discuss the major disorders of the surfactant system. The final part of the review will be focused on the potentials and complications of surfactant therapy in the treatment of some of these disorders. It is our belief that increased knowledge of the surfactant system and its functions will lead to a more optimal composition of the exogenous surfactants and, perhaps, widen their applicability to treatment of surfactant disorders other than neonatal respiratory distress syndrome.Key words: Surfactant protein-Pulmonary surfactant-Respiratory distress syndrome. HistoryResearch on surfactant goes back to 1929 when von Neergaard published the first paper about the difference in pressure needed to inflate lungs with air or with liquid [333]. He found that the pressure necessary for filling the lungs with air was higher than when the lungs were filled with liquid. To explain this result he stated that the alveoli were stabilized by lowering the naturally high surface tension of the air/water interface. In 1946 Thannhauser and co-workers reported that lung tissue has a remarkably high content of the lipid dipalmityl lecithin (current name, dipalmitoylphosphatidylcholine)Offprint requests to: Henk P. Haagsman.

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Section: Therapeutic Effects Of Hormonesmentioning

confidence: 99%

The Pulmonary Surfactant System: Biochemical and Clinical Aspects

Creuwels

Golde

Haagsman

1997

Lung

283

188

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“…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%

“…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%

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 typical type II cell morphology with increased number of lamellar bodies is seen at 19 d of fetal life (term being 22 d). At this time, DPPC and SP-A and SP-B proteins also begin to increase (8). Thus, increased production of surfactant does not occur until after 80% of gestation is completed.…”

mentioning

confidence: 96%

Leptin Enhances Lung Maturity in the Fetal Rat

et al. 2006

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Pulmonary alveolar type II cells synthesize and secrete phospholipids and surfactant proteins. In most mammalian species, the synthesis of phospholipids and proteins of lung surfactant increases with fetal lung maturation, which occurs late in gestation. Factors that may promote lung maturation and surfactant production include the placental hormone, leptin, whose expression increases with advancing gestational age. We demonstrate that physiologic concentrations of leptin (1 and 10 ng/mL) increase the levels of surfactant proteins (SP) A, B, and C mRNA as well as SP-A and SP-B protein in d-17 fetal rat lung explants in vitro. To determine whether leptin exerts similar effects in vivo, we administered leptin antenatally to pregnant rats and compared its effects to that of dexamethasone, a known mediator of fetal lung development. Antenatal treatment with leptin for 2 d significantly increased the average weight of the fetal lungs in relation to their body weight. Histologic analysis revealed that the increase in fetal lung weight was accompanied by an increase in the number and maturation of type II alveolar cells and the expression of surfactant proteins B and C in these cells. Collectively, these results suggest that leptin is a cytokine regulator of rat fetal lung maturity.

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Appearance of surfactant proteins, SP-A and SP-B, in developing rat lung and the effects of in vivo dexamethasone treatment

Cited by 47 publications

References 32 publications

The Pulmonary Surfactant System: Biochemical and Clinical Aspects

The Pulmonary Surfactant System: Biochemical and Clinical Aspects

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

Leptin Enhances Lung Maturity in the Fetal Rat

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