| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |

Cardiovascular Research Institute and Departments of Pediatrics and Medicine, University of California San Francisco 94143
W. Alton Jones Cell Science Center Lake Placid, New York 12946
Address all correspondence and reprint requests to: P. L. Ballard, Cardiovascular Research Institute, University of California, San Francisco, California 94143.
Abstract
Synthesis of surfactant in the lung of fetal, and perhaps adult, animals responds to glucocorticoids, and glucocorticoid receptor activity has been identified in this tissue of several species. To determine whether receptor is present in the alveolar type II cell, which is the site of surfactant production, we studied glucocorticoid binding by various populations of lung cells.
Specific binding was demonstrated in freshly isolated populations of rat lung cells containing primarily alveolar type II cells, in organotypic cultures derived from fetal rat lung containing 90% type II cells, in cultured A549, L-2, and F-42 cell lines which apparently originated from type II cells, and in human lung fibroblastic cells. The equilibrium dissociation constants for nuclear binding of dexamethasone by intact cells at 37 C ranged from 5.0–10.8 nM, and the number of binding sites per cell ranged from 5,700–57,000. In cytosol preparations from L-2 and A549 cells, there was equivalent specific binding of both natural and synthetic corticosteroids, and binding activity had the expected specificity for steroids with glucocorticoid activity.
These findings indicate that glucocorticoid receptor is present in both fetal and adult pulmonary type II cells and in cell lines which apparently originated from these cells. The presence of receptor in type II cells is consistent with a direct action of glucocorticoids on these cells in vivo. (Endocrinology 102: 1570, 1978)
Footnotes
* This study was supported by Program Project Grant HL-06285 and Pulmonary Specialized Centers of Research Grants HL-14201 and HL-19185 from the NHLBI.
Established Investigator of the AHA.
Received September 19, 1977.
This article has been cited by other articles:
![]() |
S. Sai, C. L. Esteves, V. Kelly, Z. Michailidou, K. Anderson, A. P. Coll, Y. Nakagawa, T. Ohzeki, J. R. Seckl, and K. E. Chapman Glucocorticoid Regulation of the Promoter of 11{beta}-Hydroxysteroid Dehydrogenase Type 1 Is Indirect and Requires CCAAT/Enhancer-Binding Protein-{beta} Mol. Endocrinol., September 1, 2008; 22(9): 2049 - 2060. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. N. Samtani, N. A. Pyszczynski, D. C. DuBois, R. R. Almon, and W. J. Jusko Modeling Glucocorticoid-Mediated Fetal Lung Maturation: I. Temporal Patterns of Corticosteroids in Rat Pregnancy J. Pharmacol. Exp. Ther., April 1, 2006; 317(1): 117 - 126. [Abstract] [Full Text] [PDF] |
||||
![]() |
J.-C. Wang, M. K. Derynck, D. F. Nonaka, D. B. Khodabakhsh, C. Haqq, and K. R. Yamamoto From The Cover: Chromatin immunoprecipitation (ChIP) scanning identifies primary glucocorticoid receptor target genes PNAS, November 2, 2004; 101(44): 15603 - 15608. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Jain, X.-J. Chen, S. Ramosevac, L. A. Brown, and D. C. Eaton Expression of highly selective sodium channels in alveolar type II cells is determined by culture conditions Am J Physiol Lung Cell Mol Physiol, April 1, 2001; 280(4): L646 - L658. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. R. Provost, C. H. Blomquist, C. Godin, X.-F. Huang, N. Flamand, V. Luu-The, D. Nadeau, and Y. Tremblay Androgen Formation and Metabolism in the Pulmonary Epithelial Cell Line A549: Expression of 17{beta}-Hydroxysteroid Dehydrogenase Type 5 and 3{alpha}-Hydroxysteroid Dehydrogenase Type 3 Endocrinology, August 1, 2000; 141(8): 2786 - 2794. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |