Time of Appearance of Lung Surfactant in the Fœtal Mouse

Buckingham, Sue; Avery, Mary Ellen

doi:10.1038/193688a0

Cited by 168 publications

(63 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This might appear as increased synthetic activity. The time of gestation in the fetal mouse that we studied is consistent with this hypothesis, as abundant surfactant stores normally become apparent on electron micrographs on day 18 of gestation (32). Further studies of lamellar body-specific phospholipids will be important for resolving this question.…”

Section: Discussionsupporting

confidence: 73%

Delayed Lung Maturation in the Macrosomic Offspring of Genetically Determined Diabetic (db/+) Mice1

1989

View full text Add to dashboard Cite

ABSTRACT. We studied a genetically determined diabetes in pregnancy, the heterozygous diabetes (db/+) mouse. We found that fetal mice from these pregnancies are macrosomic with increased body, lung, and placenta wt, have altered organ protein, DNA and phospholipid content, and exhibit abnormal carbohydrate metabolism with increased liver and glycogen content. We further studied the effect of increased substrate availability and utilization on lung growth and maturation in (db/+) fetal mice, by measuring lung phospholipid synthesis as represented by the incorporation of the radiolabeled precursors, [3H] The increased synthesis of lung disaturated phosphatidylcholine in diabetic fetal mice may reflect the enhancement of body and lung growth in these macrosomic fetuses. Lung maturation, as represented by phosphatidylglycerol synthesis, the phosphatidylglycerol/phosphatidylinositol ratio, and morphologic indices, was abnormal in diabetic fetuses. The diabetic mouse is a useful model for studying the mechanisms resulting in enhanced growth and concomitant alterations in lung maturation in the infant of a diabetic mother. (Pediatr Res 25:173-179, 1989) Abbreviations RDS, respiratory distress syndrome PC, phosphatidylcholine SPC, disaturated phosphatidylcholine S, sphingomyelin PI, phosphatidylinositol PE, phosphatidylethanolamine PS, phosphatidylserine PG, phosphatidylglycerol Human fetal development during maternal diabetes is abnormal, frequently resulting in obese, macrosomic newborns with delayed maturation of various organ systems. Infants of diabetic mothers whose hyperglycemia is inadequately controlled late in gestation appear to have an increased risk of lung immaturity, as manifested by RDS at birth (I). Animal models in which maternal glucose intolerance and consequent fetal hyperglycemia are artificially induced have been developed to study this phenomenon (2). However, important questions concerning maternal-fetal interactions in diabetes and the consequent effects on fetal organ growth and development might be more appropriately addressed by using a model in which the diabetes is genetically determined, therefore occuning spontaneously in the mother (2).The diabetic mouse (db/db) is a well-described model of genetic diabetes transferred as an autosomal recessive trait. Homozygous (db/db) animals exhibit visible obesity in infancy with marked hyperglycemia and insulin resistance, followed later by hypoinsulinemia and profound diabetes at 3-4 mo of age (3). As the adult (db/db) mouse is infertile, heterozygous animals must be bred to produce offspring. The heterozygous female (db/ +) exhibits normal glucose tolerance except during pregnancy, when abnormal glucose tolerance, postprandial hyperglycemia and elevated Hb A 1C levels are present (4,5).We have studied the fetus of the pregnant heterozygous (db/ +) female to learn more about growth and the development during pregnancy complicated by abnormal glucose metabolism. In this report, we describe our results in characterizing abnormal fetal growth duri...

show abstract

Section: Discussionsupporting

confidence: 73%

Delayed Lung Maturation in the Macrosomic Offspring of Genetically Determined Diabetic (db/+) Mice1

1989

View full text Add to dashboard Cite

show abstract

“…A correlation has already been shown between pressure-volume deflation curves and surface balance results in the lungs of babies (Gruenwald et al 1962) and in lambs (Buckingham & Avery, 1962), rats and guinea-pigs (Pattle, 1961 , no close relationship appears to exist in the gestation of rabbits between the loss of cuboidal alveolar epithelium and the appearance of surfactant as reported in guinea-pigs and rats by Pattle (1961). Short (1951) showed that cuboidal epithelium disappears in the rabbit between the 24th and 26th days of gestation, whereas surfactant does not appear in functional amounts until the 28th day.…”

Section: Asphyxiated Animalsmentioning

confidence: 96%

“…The low surface tension, characteristic of normal lung extracts, appears to develop in the last 15 % of gestation in the mouse (Buckingham & Avery, 1962), guinea-pig, rat (Pattle, 1961) and lamb (Howatt, Avery, Humphreys, Normand, Reid & Strang, 1965; Orzalesi, Motoyama, Jacobson, Kikkawa, Reynolds & Cook, 1965). In these studies gestational age was usually calculated indirectly from the histological appearance of the lungs or from the length and weight of the foetus.…”

Section: Introductionmentioning

confidence: 99%

Effects of gestation and prenatal asphyxia on pulmonary surface properties of the foetal rabbit*

Humphreys¹,

Strang²

1967

The Journal of Physiology

View full text Add to dashboard Cite

SUMMARY1. The pulmonary surface properties of foetal rabbits were studied after delivery by Caesarean section at 26-30 days and after normal delivery at term (31 days).2. Quasi-static pressure-volume curves were defined for the lungs and the surface properties of the same lungs were further studied both by the bubble-stability method and by means of a surface balance and trough. Results given by each method are compared and discussed.3. At the 26th day of gestation the pulmonary surface properties, characteristic of the animal at term, were not yet present. These properties were first evident on the 28th day.4. A period of 16 min intense prenatal asphyxia on the 28th day of gestation failed to produce a change in pulmonary surface properties.

show abstract

“…This occurs on gestation day (GD) 17 . 5 in the mouse as indicated by the appearance of lamellar bodies (Buckingham & Avery 1962), an increase in surface activity in the mouse lung homogenate (Buckingham & Avery 1962), and by increases in the activity of some enzymes involved in pulmonary lipid metabolism (Oldenberg & Van Golde 1977, Brehier & Rooney 1981. From the list of genes obtained by microarray hybridization experiments and presenting a sex difference in expression, two groups of genes were of particular interest.…”

Section: Introductionmentioning

confidence: 99%

Apolipoprotein A-I, A-II, C-II, and H expression in the developing lung and sex difference in surfactant lipids

Provost¹,

Boucher²,

Tremblay³

2008

Journal of Endocrinology

View full text Add to dashboard Cite

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 receptordependent. 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 (PZ0 . 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 apoHmRNA 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 17b-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.

show abstract

Time of Appearance of Lung Surfactant in the Fœtal Mouse

Cited by 168 publications

References 7 publications

Delayed Lung Maturation in the Macrosomic Offspring of Genetically Determined Diabetic (db/+) Mice1

Delayed Lung Maturation in the Macrosomic Offspring of Genetically Determined Diabetic (db/+) Mice1

Effects of gestation and prenatal asphyxia on pulmonary surface properties of the foetal rabbit*

Apolipoprotein A-I, A-II, C-II, and H expression in the developing lung and sex difference in surfactant lipids

Contact Info

Product

Resources

About