Differential Glucocorticoid Regulation of the Pulmonary Hydrophobic Surfactant Proteins SP-B and SP-C

Venkatesh, Vugranam C.; Iannuzzi, Debra M.; Ertsey, Robert; Ballard, Philip L.

doi:10.1165/ajrcmb/8.2.222

Cited by 73 publications

(47 citation statements)

References 25 publications

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“…There is also a dexamethasone-induced pre-and postnatal increase of the production of SP-D, an effect that is absent when dexamethasone is administered to adult rats [229]. The extent of regulation of SP-C mRNA is still under debate, varying from no increase [48] to a 35-fold increase of SP-C mRNA compared with a control group [326]. Differential glucocorticoid regulation of both hydrophobic proteins has been reported [77,326].…”

Section: Therapeutic Effects Of Hormonesmentioning

confidence: 99%

“…The extent of regulation of SP-C mRNA is still under debate, varying from no increase [48] to a 35-fold increase of SP-C mRNA compared with a control group [326]. Differential glucocorticoid regulation of both hydrophobic proteins has been reported [77,326]. There is still discussion regarding by which mechanisms corticosteroids accelerate surfactant lipid synthesis [9, 268,282].…”

Section: Therapeutic Effects Of Hormonesmentioning

confidence: 99%

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The Pulmonary Surfactant System: Biochemical and Clinical Aspects

Creuwels

Golde

Haagsman

1997

Lung

282

188

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Abstract. This article starts with a brief account of the history of research on pulmonary surfactant. We will then discuss the morphological aspects and composition of the pulmonary surfactant system. We describe the hydrophilic surfactant proteins A and D and the hydrophobic surfactant proteins B and C, with focus on the crucial roles of these proteins in the dynamics, metabolism, and functions of pulmonary surfactant. Next we discuss the major disorders of the surfactant system. The final part of the review will be focused on the potentials and complications of surfactant therapy in the treatment of some of these disorders. It is our belief that increased knowledge of the surfactant system and its functions will lead to a more optimal composition of the exogenous surfactants and, perhaps, widen their applicability to treatment of surfactant disorders other than neonatal respiratory distress syndrome.Key words: Surfactant protein-Pulmonary surfactant-Respiratory distress syndrome. HistoryResearch on surfactant goes back to 1929 when von Neergaard published the first paper about the difference in pressure needed to inflate lungs with air or with liquid [333]. He found that the pressure necessary for filling the lungs with air was higher than when the lungs were filled with liquid. To explain this result he stated that the alveoli were stabilized by lowering the naturally high surface tension of the air/water interface. In 1946 Thannhauser and co-workers reported that lung tissue has a remarkably high content of the lipid dipalmityl lecithin (current name, dipalmitoylphosphatidylcholine)Offprint requests to: Henk P. Haagsman.

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Section: Therapeutic Effects Of Hormonesmentioning

confidence: 99%

Section: Therapeutic Effects Of Hormonesmentioning

confidence: 99%

The Pulmonary Surfactant System: Biochemical and Clinical Aspects

Creuwels

Golde

Haagsman

1997

Lung

282

188

View full text Add to dashboard Cite

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“…SP-B gene expression is increased by glucocorticoids and cAMP in cultured explants of rat and human lung, and by in vivo glucocorticoid treatment in fetal rats and rabbits (1, 7, 9 -11). The glucocorticoid responses in human lung and NeI H-441 cells, which are derived from a human lung adenocarcinoma, involve both increased rate of gene transcription and stabilization of SP-B mRNA (12,13).…”

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confidence: 99%

Surfactant Protein B in Human Fetal Lung: Developmental and Glucocorticoid Regulation

et al. 1995

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ABSTRAGT Vol. 38, No.5, 1995 Printed ill U.S.A.Pulm onary surfac tant protein B (SP-B) enhances phospholip id film formation in vitro and is essential for normal surfactant functio n in vivo. We examined hum an fetal lung before and during explant culture for content and cellular localization of SP-B mRNA and prote in. SP-B mRNA was low in preculture specime ns (18 -20 wk) but hybridization signal increased ove r epithelial cells dur ing culture and was enha nced by dexa methasone treatment (10 nM). SP-B immunofluorescence was very low in preculture specimens, increased duri ng culture, and was uniformly intense in epithelial cells of dexam ethasone-treated tissue. With a newly developed immunoassay, SP-B protein was undetectable in preculture lung «2% of adult), appeared during culture (26 % of adul t), and was furth er increased~3-fo ld by dexamethasone treatment (86 % of adult); lung tissu e of two newborn infants contained 7-9-fold more SP-B than is found in the adult. Using Western blot with enhanced chemiluminescence, mature SP-B was undetectable in 16-wk specimens but was Pulmonary surfactant isolated from bronchoalveolar lavage fluid contains a variety of lipids and proteins. Three SP have been identified that influence surfactant structure, function, or metabolism. SP-A is a hydrophili c protein of 28 -36-kD monomer size that has a numb er of demonstrated effects on surfactant in vitro both alone and interacting with other surfactant proteins. SP-B and SP-C are lipophilic proteins of approx imately 8 and 4 kD, respectively, that co-isolate with surfactant lipids. Both of these proteins enhance the rate of phospholipid film formation and improve the surface activity of lipid mixtures in vivo (rev iewed in Ref. 1).SP-B appears to be critically important for surfactant function in vivo. Antib odies to SP-B inactivate a replacement surfactant prepared from pig lungs and cause severe respiratory Received November 17, 1994; accepted May 9, 1995 present in 19-24-wk preculture tissue at 0.2-2.9% of the adult level. By comparison, SP-B mRNA content is 14 and 50 % of adult leve l in 19-and 24-wk lung tissue, respec tively; levels increase 3-fold during culture and a further 3-fold with dexamethason e. Based on these observed differences between mRNA and protein content, we conclude that basal SP-B gene exp ression in epithe lial ce lls of hum an fetal lung is regulated primarily at the level of translatio n or prote in stabil ity, where as glucocorticoids act transc riptionally. We specu late that SP-B protein acc umulates only as type II cells differentiate and acquire lamellar bodies for processing and storage of SP-B. (Pediatr R es 38: 668-675, 1995) Abbreviations SP , surfactant protein TBS, Tris-buffered salin e distress when instilled into the trachea of newborn animals or inoculated intraperitoneally into adult mice (2-4). In pulmonary function studies with preterm rabbits, Rider et al. (5) found that the activity of lipid-SP-B preparations was equivalent to that of natural surfactan t. Recently, Nog...

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“…Since both SP-B and SP-C expression are TTF-1-dependent and their transcripts have relatively similar half lives [16], a stronger transcription complex may be required for SP-C expression in the lung. Our ChIP and quantitative RT-PCR studies suggests that PLAGL2 association with the SP-C promoter in chromatin could further up regulate its activity in vivo (Figures 4). TTF-1 expression is impaired in lung epithelial cells during the acute lung injury [17] or in cells under an oxidative stress condition (Figures 1 and 2).…”

Section: Discussionmentioning

confidence: 99%

PLAGL2 translocation and SP-C promoter activity—A cellular response of lung cells to hypoxia

Guo¹,

Yang²,

Weissler³

et al. 2007

Biochemical and Biophysical Research Communications

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Cobalt is a transition metal which can substitute for iron in the oxygen-sensitive protein and mimic hypoxia. Cobalt was known to be associated with the development of lung disease. In this study, when lung cells were exposed to hypoxia induced by CoCl 2 at a sub-lethal concentration (100 μM), their thyroid transcription factor-1 (TTF-1) expression was greatly reduced. Under this condition, SP-B promoter activity was down regulated, but SP-C promoter remained active. Therefore, we hypothesized that other factor(s) besides TTF-1 might contribute to the modulation of SP-C promoter in hypoxic lung cells. Pleomorphic adenoma gene like-2 (PLAGL2), a previously identified TTF-1-independent activator of the SP-C promoter, was not down regulated, nor increased, within those cells. Its cellular location was redistributed from the cytoplasm to the nucleus. Chromatin immunoprecipitation (ChIP) and quantitative RT-PCR analyses demonstrated that nuclear PLAGL2 occupied and transactivated the endogenous SP-C promoter in lung cells. Thereby, through relocating and accumulating of PLAGL2 inside the nucleus, PLAGL2 interacted with its target genes for various cellular functions. These results further suggest that PLAGL2 is an oxidative stress responding regulator in lung cells.

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Differential Glucocorticoid Regulation of the Pulmonary Hydrophobic Surfactant Proteins SP-B and SP-C

Cited by 73 publications

References 25 publications

The Pulmonary Surfactant System: Biochemical and Clinical Aspects

The Pulmonary Surfactant System: Biochemical and Clinical Aspects

Surfactant Protein B in Human Fetal Lung: Developmental and Glucocorticoid Regulation

PLAGL2 translocation and SP-C promoter activity—A cellular response of lung cells to hypoxia

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