Lung surfactant.

Rooney, Seamus A.

doi:10.1289/ehp.8455205

Cited by 44 publications

(17 citation statements)

References 334 publications

(304 reference statements)

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“…PA de novo biosynthesis utilizes dihydroxyacetone phosphate (DHAP) derived from glucose or glycogen that is then processed into PA by two different pathways both of which are active in the lung [30, 31]. It was shown that fetal type II cell precursors accumulate significant amounts of glycogen that are used as a carbon source, providing chemical energy and serving as an important precursor for PA and surfactant synthesis [32].…”

Section: Synthesis and Regulation Of Surfactant Phospholipidsmentioning

confidence: 99%

“…Endogenous glucocorticoids directly affect fetal lung maturation via glucocorticoid receptors identified in the type II alveolar cells [8, 247, 248]. Glucocorticoids also exert stimulatory effects on regulatory enzymes (CTP, CPT, PAP, glycerophosphate phosphatidyltransferase and phosphatidylglycerophosphatase) involved in phospholipid biosynthesis [9, 31]. Thyroid hormone also accelerates lung maturation and increases surfactant PC biosynthesis [8, 31, 249].…”

Section: Modulators Of Surfactant Production In Lung Diseasementioning

confidence: 99%

“…Glucocorticoids also exert stimulatory effects on regulatory enzymes (CTP, CPT, PAP, glycerophosphate phosphatidyltransferase and phosphatidylglycerophosphatase) involved in phospholipid biosynthesis [9, 31]. Thyroid hormone also accelerates lung maturation and increases surfactant PC biosynthesis [8, 31, 249]. Estrogens upregulate maturation of the fetal lung via increasing CCT activity and lysolecithin acyltransferase activity, and these hormones impact postnatal lung development and lung cancer progression [31, 250, 251].…”

Section: Modulators Of Surfactant Production In Lung Diseasementioning

confidence: 99%

“…Thyroid hormone also accelerates lung maturation and increases surfactant PC biosynthesis [8, 31, 249]. Estrogens upregulate maturation of the fetal lung via increasing CCT activity and lysolecithin acyltransferase activity, and these hormones impact postnatal lung development and lung cancer progression [31, 250, 251]. In contrast, androgens and insulin have been implicated as inhibitory signals for surfactant phospholipid synthesis [9, 31, 252].…”

Section: Modulators Of Surfactant Production In Lung Diseasementioning

confidence: 99%

“…Estrogens upregulate maturation of the fetal lung via increasing CCT activity and lysolecithin acyltransferase activity, and these hormones impact postnatal lung development and lung cancer progression [31, 250, 251]. In contrast, androgens and insulin have been implicated as inhibitory signals for surfactant phospholipid synthesis [9, 31, 252]. A fibroblast-pneumocyte factor stimulates PC, DPPC and PG synthesis in the fetal type II cells [9].…”

Section: Modulators Of Surfactant Production In Lung Diseasementioning

confidence: 99%

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Surfactant phospholipid metabolism

Agassandian

Mallampalli

2013

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

193

176

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Pulmonary surfactant is essential for life and is comprised of a complex lipoprotein-like mixture that lines the inner surface of the lung to prevent alveolar collapse at the end of expiration. The molecular composition of surfactant depends on highly integrated and regulated processes involving its biosynthesis, remodeling, degradation, and intracellular trafficking. Despite its multicomponent composition, the study of surfactant phospholipid metabolism has focused on two predominant components, disaturated phosphatidylcholine that confers surface-tension lowering activities, and phosphatidylglycerol, recently implicated in innate immune defense. Future studies providing a better understanding of the molecular control and physiological relevance of minor surfactant lipid components are needed.

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Section: Synthesis and Regulation Of Surfactant Phospholipidsmentioning

confidence: 99%

Section: Modulators Of Surfactant Production In Lung Diseasementioning

confidence: 99%

Section: Modulators Of Surfactant Production In Lung Diseasementioning

confidence: 99%

Section: Modulators Of Surfactant Production In Lung Diseasementioning

confidence: 99%

Section: Modulators Of Surfactant Production In Lung Diseasementioning

confidence: 99%

See 3 more Smart Citations

Surfactant phospholipid metabolism

Agassandian

Mallampalli

2013

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

193

176

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Cytoplasmic bar‐like structures of alveolar type II cells: An ultrastructural study in freshly isolated cells from rat lungs

Vincent

Nadeau

1987

Am. J. Anat.

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Bar-like structures are tubular cytoplasmic inclusions found in situ in pulmonary epithelial type II cells of several animal species. The physiological significance and mode of formation of these inclusions are not fully established. In this paper, we describe bar-like structures as found in freshly isolated type II cells from rat lungs. Pulmonary cells were dissociated from the tissue with elastase and separated on a discontinuous density gradient of Percoll. The complete isolation procedure yielded 17 X 10(6) type II cells per animal (purity = 80%). Either from the crude cell suspensions or the purified preparations, only a small fraction of the type II cell population harbored the inclusions (less than 5%). It is shown that the bounding membranes of the bar-like structures can derive from the endoplasmic reticulum, the nuclear membrane, or the Golgi apparatus. Occasional connections with lamellar bodies were observed, and different levels of complexity in the bar-like structures were also found. The apparent rigid conformation and the orientation of the bar-like structures were taken as evidence for a role of the cytoskeleton in their formation. Because the inclusions do not appear to be new organelles or cellular structures performing a specific function, we propose that their formation may be a transient and limited cellular event in normal cells. However, the stabilization and the generation of the osmiophilic structures, as well as their overproduction, may reflect alterations of the normal physiology of the type II cells.

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A putative adverse outcome network for neonatal mortality and lower birth weight in rodents: Applicability to per‐ and polyfluoroalkyl substances and relevance to human health

Rogers

Heintz

Thompson

et al. 2023

Birth Defects Research

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Background Some per‐ and poly‐fluoroalkyl substances (PFAS) cause neonatal mortality and lower birth weight in rodents. We constructed an Adverse Outcome Pathway (AOP) network for neonatal mortality and lower birth weight in rodents, comprising three putative AOPs. We then assessed strengths of the evidence for the AOPs and applicability to PFAS. Finally, we considered the relevance of this AOP network to human health. Methods Literature searches targeted PFAS, peroxisome proliferator‐activated receptor (PPAR) agonists, other nuclear receptors, relevant tissues, and developmental targets. We used reviews of established biology and described results of studies with prenatal PFAS exposure that assessed birth weight and neonatal survival. Molecular initiating events (MIEs) and key events (KEs) were proposed and strengths of KE relationships (KERs), applicability to PFAS, and human relevance were assessed. Results Neonatal mortality has been observed in rodents following gestational exposure to most longer chain PFAS studied, often coincident with lower birth weight. In AOP 1, PPARα activation and PPARγ activation or downregulation are MIEs; placental insufficiency, fetal nutrient restriction, neonatal hepatic glycogen deficit, and hypoglycemia are KEs leading to neonatal mortality and lower birth weight. In AOP 2, constitutive androstane receptor (CAR) and pregnane X receptor (PXR) activation upregulates Phase II metabolism, lowering maternal circulating thyroid hormones. In AOP 3, disrupted pulmonary surfactant function and PPARγ downregulation cause neonatal airway collapse and mortality from respiratory failure. Conclusions It is likely that different components of this AOP network will apply to different PFAS, largely determined by which nuclear receptors they activate. The MIEs and KEs in this AOP network can occur in humans, but differences in PPAR structure and function, and the timeline of liver and lung development, suggest that humans may be less susceptible to this AOP network. This putative AOP network elucidates knowledge gaps and research needed to better understand the developmental toxicity of PFAS.

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Lung surfactant.

Cited by 44 publications

References 334 publications

Surfactant phospholipid metabolism

Surfactant phospholipid metabolism

Cytoplasmic bar‐like structures of alveolar type II cells: An ultrastructural study in freshly isolated cells from rat lungs

A putative adverse outcome network for neonatal mortality and lower birth weight in rodents: Applicability to per‐ and polyfluoroalkyl substances and relevance to human health

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