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Physiol. Genomics 4: 51-57, 2000;
1094-8341/00 $5.00
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Received 8 June 2000; accepted in final form 13 September 2000.
Physiological Genomics 4:51-57 (2000)
1094-8341/00 $5.00 © 2000 American Physiological Society

Retinoic acid receptor-ß: an endogenous inhibitor of the perinatal formation of pulmonary alveoli

GLORIA DE CARLO MASSARO1, DONALD MASSARO2, WAI-YEE CHAN1, LINDA B. CLERCH1, NORBERT GHYSELINCK3, PIERRE CHAMBON3 and ROSHANTHA A. S. CHANDRARATNA4

1 Lung Biology Laboratory, Department of Pediatrics, Georgetown University School of Medicine, Washington District of Columbia 20007-2197
2 Lung Biology Laboratory, Department of Medicine, Georgetown University School of Medicine, Washington District of Columbia 20007-2197
3 Institut de Génétique et de Biologie Moléculaire et Cellulaire, 67404 Illkirch, Strasbourg, France
4 Retinoid Research, Allergan, Inc., Irvine, California 92623-9534

Pulmonary alveoli are formed, in part, by subdivision (septation) of the gas-exchange saccules of the immature lung. Septation is developmentally regulated, and failure to septate at the appropriate time is not followed by delayed spontaneous septation. We report retinoic acid receptor (RAR) ß knockout mice exhibit premature septation; in addition, they form alveoli twice as fast as wild-type mice during the period of septation but at the same rate as wild-type mice thereafter. Consistent with the perinatal effect of RARß knockout, RARß agonist treatment of newborn rats impairs septation. These results 1) identify RARß as the first recognized endogenous signaling that inhibits septation, 2) demonstrate premature onset of septation may be induced, and 3) show the molecular signaling regulating alveolus formation differs during and after the period of septation. Suppressing perinatal RARß signaling by RARß antagonists may offer a novel, nonsurgical, means of preventing, or remediating, failed septation in prematurely born children.

bronchopulmonary dysplasia; mice; knockout; very low birth weight infant; pulmonary emphysema; morphogenesis




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