TGF-beta3-null mutation does not abrogate fetal lung maturation in vivo by glucocorticoids

Newborn transforming growth factor (TGF)-beta3-null mutant mice exhibit defects of palatogenesis and pulmonary development. Glucocorticoids, which play a central role in fetal lung maturation, have been postulated to mediate their stimulatory effects on tropoelastin mRNA expression through TGF-beta3 in cultured lung fibroblasts. In the present study, we analyzed the abnormally developed lungs in TGF-beta3-null mutant mice and compared the effects of glucocorticoids on gene expression and lung morphology between TGF-beta3 knockout and wild-type mice. Lungs of TGF-beta3-null mutant mice on embryonic day 18.5 did not form normal saccular structures and had a thick mesenchyme between terminal air spaces. Moreover, the number of surfactant protein C-positive cells was decreased in TGF-beta3-null mutant lungs. Interestingly, glucocorticoids were able to promote lung maturation and increased expression of both tropoelastin and fibronectin but decreased the relative number of surfactant protein C-positive cells in fetal lungs of both genotypes. This finding provides direct evidence that glucocorticoid signaling in the lung can use alternative pathways and can exert its effect without the presence of TGF-beta3.

Medienart:

E-Artikel

Erscheinungsjahr:

1999

Erschienen:

1999

Enthalten in:

Zur Gesamtaufnahme - volume:277

Enthalten in:

The American journal of physiology - 277(1999), 6 vom: 17. Dez., Seite L1205-13

Sprache:

Englisch

Beteiligte Personen:

Shi, W [VerfasserIn]
Heisterkamp, N [VerfasserIn]
Groffen, J [VerfasserIn]
Zhao, J [VerfasserIn]
Warburton, D [VerfasserIn]
Kaartinen, V [VerfasserIn]

Links:

Volltext

Themen:

7S5I7G3JQL
Dexamethasone
Fibronectins
Glucocorticoids
Journal Article
Proteolipids
Pulmonary Surfactants
RNA, Messenger
Research Support, U.S. Gov't, P.H.S.
Transforming Growth Factor beta
Tropoelastin

Anmerkungen:

Date Completed 20.01.2000

Date Revised 28.08.2018

published: Print

Citation Status MEDLINE

doi:

10.1152/ajplung.1999.277.6.L1205

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM105306800