Influence of the Major Histocompatibility Complex (H-2) on Glucocorticoid-Stimulated Pulmonary Surfactant Synthesis in Two Congenic Mouse Strains

Ls, Honig; Bt, Smith; Hc, Slavkin; Hg, Donahue

doi:10.3181/00379727-176-41892

Cited by 5 publications

(4 citation statements)

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“…Pregnant females were housed in separate cages. Embryos were dissected from uterine decidua and developmentally staged by external features according to Theiler [81] and as previously described [44]. Our studies cover Theiler stages 19-27 (11-18 days gestation, E l l d-El8d).…”

Section: Methodsmentioning

confidence: 99%

“…Using an Olympus BH series microscope, a Dage MTI 65 video camera, and an ImageMaster lo00 Image Analysis System by Technology Resources, Inc. (Nashville, Tenn., USA), [43][44][45][46][47][48][49][50][51][52][53][54][55][56][57][58][59] was recorded as a x 700 magnification image from which measurements of the branching epithelia were performed. Epon sections (1 pm) were stained with Toluidine blue and used to determine timedependent changes in the epithelial thickness during embryonic lung morphogenesis in vivo and in vitro.…”

Section: Sp-35 Antiserum Preparationmentioning

confidence: 99%

“…Exogenous mitogenic factors found within fetal calf sera, as well as thyroxin and glucocorticosteroid hormones, appear to increase or enhance embryonic and fetal marnmalian lung development as well as type I1 cytodifferentiation [7-9, 35-50, [41][42]44,57,[71][72][73]. Glucocorticoids increase the production of enzymes involved in phospholipid metabolism [58-591, production of disaturated phosphatidyl choline [22,[35][36][37]44, 731, expression of pulmonary surfactant (SP-35) gene products [6-91, and formation of lamellar bodies (LB) [42, 531. At what time and in what sequence these processes involved in surfactant production are activated, and how they are coupled to form an optimally functioning lung, is not yet known.…”

Section: Introductionmentioning

confidence: 99%

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Lamellar body formation precedes pulmonary surfactant apoprotein expression during embryonic mouse lung development in vivo and in vitro

et al. 1989

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Section: Methodsmentioning

confidence: 99%

Section: Sp-35 Antiserum Preparationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Lamellar body formation precedes pulmonary surfactant apoprotein expression during embryonic mouse lung development in vivo and in vitro

et al. 1989

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“…Female B10. A/SnSgJ mice, which were obtained from Jackson Laboratory (Bar Harbor, Maine), were placed overnight with males [27]. The presence of a vaginal plug was considered to be day 0 of pregnancy.…”

Section: Methodsmentioning

confidence: 99%

Ultrastructural and immunofluorescence studies of basal-lamina alterations during mouse-lung morphogenesis

Jaskoll

Slavkin

1984

Differentiation

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Mouse major histocompatibility complex (H‐2) and fetal lung development: Implications for human pulmonary maturation

Jaskoll

Minkin

et al. 1990

Am. J. Med. Genet.

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Using C57/10Sn (B10, H-2b) and B10.A/SgSn (B10.A,H-2a) congenic mice, we measured 1) the level of endogenous pulmonary corticosterone during mouse development; 2) the degree of lung morphological maturation on gestation day 17, with or without corticosteroid treatment; and 3) the maternal influence on normal lung development and fetal response to corticosteroids. The results of our study indicate that there was a progressive increase in the level of endogenous hormone with time in fetal B10 (H-2b) and B10.A (H-2a) mice; throughout mid- to late gestation, the detectable amount of hormone was almost identical in lungs of both strains. Evaluating the degree of lung maturation by morphometry, B10.A mouse lungs were found to be less mature than B10 mouse lungs. Following corticosteroid treatment on day 12 of gestation, H-2a lungs were equal to or more mature than H-2b lungs. We also compared heterozygous mouse lungs from reciprocal crosses (B10.B10.A, b/a and B10.A.B10, a/b). Mice with a maternally derived H-2a haplotype had less mature lungs than those with a maternally derived H-2b haplotype, suggesting a maternal effect. When exogenous hormone was administered, all heterozygous mouse lungs increased in maturity regardless of the origin of the H-2a haplotype. The treated a/b or b/a lungs were more mature than homozygous b/b and less mature than homozygous a/a lungs. We conclude that progressive lung maturation is associated with a gene(s) at or near the H-2 complex, as is the ability to respond to corticosteroids.

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Influence of the Major Histocompatibility Complex (H-2) on Glucocorticoid-Stimulated Pulmonary Surfactant Synthesis in Two Congenic Mouse Strains

Cited by 5 publications

References 0 publications

Lamellar body formation precedes pulmonary surfactant apoprotein expression during embryonic mouse lung development in vivo and in vitro

Lamellar body formation precedes pulmonary surfactant apoprotein expression during embryonic mouse lung development in vivo and in vitro

Ultrastructural and immunofluorescence studies of basal-lamina alterations during mouse-lung morphogenesis

Mouse major histocompatibility complex (H‐2) and fetal lung development: Implications for human pulmonary maturation

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