Phospholipid synthesis in isolated alveolar type II cells exposed <i>in vitro</i> to paraquat and hyperoxia

Haagsman, Henk P.; Schuurmans, E. A. J. M.; Batenburg, Joseph J.; Golde, L.M.G. Van

doi:10.1042/bj2450119

Cited by 14 publications

(5 citation statements)

References 25 publications

(3 reference statements)

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“…These proliferating type II cells have a decreased lamellar body pool size (19), which is consistent with a decreased synthesis of surfactant. Second, production or secretion of phospholipids and SP-A by type II cells can be impaired by reactive oxygen metabolites and cytokines (20)(21)(22)(23), which are generated after lung transplantation (24,25). Both these mechanisms may have induced the changes of surfactant that we measured at 1 wk after the initial transplantation injury in the present study.…”

Section: Discussionmentioning

confidence: 74%

Effects of Early Surfactant Treatment Persisting for One Week after Lung Transplantation in Rats

Erasmus

Hofstede

Petersen

et al. 1997

Am J Respir Crit Care Med

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We investigated whether pulmonary surfactant in rat lung transplants recovered during the first week post-transplantation, along with symptoms of the reimplantation response, and whether this recovery was affected by early surfactant treatment. The severity of pulmonary injury was varied by transplanting left lungs with 6-h and 20-h ischemia (n = 12 and 19, respectively). Half of the transplants were treated by instillation of surfactant before reperfusion. Lungs from sham operated, and normal rats (n = 4 and 5, respectively) served as controls. The pulmonary injury severely impaired lung transplant function; 10 of the worst affected animals died. After 1 wk, symptoms of reimplantation response and properties of pulmonary surfactant were assessed. If untreated, the reimplantation response had almost resolved in the 6-h but not in the 20-h ischemia group; pulmonary surfactant, however, continued to be deficient in both ischemia groups (low amounts of surfactant phospholipids and surfactant protein A [SP-A]). Surfactant treatment improved the recovery from injury in the 20-h ischemia group resulting in normal lung function and amounts of surfactant phospholipids. Amounts of SP-A were not improved by surfactant treatment. In conclusion, early surfactant treatment enhances recovery from transplantation injury and is persistently beneficial for pulmonary surfactant in lung transplants.

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Section: Discussionmentioning

confidence: 74%

Effects of Early Surfactant Treatment Persisting for One Week after Lung Transplantation in Rats

Erasmus

Hofstede

Petersen

et al. 1997

Am J Respir Crit Care Med

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“…These proliferating type II cells have a decreased lamellar body pool size (19) which is consistent with a decreased synthesis of surfactant. Second, production or secretion of phospholipids and SP-A by type II cells can be impaired by reactive oxygen metabolites and cytokines (20)(21)(22)(23) which are generated after lung transplantation (24,25). Both these mechanisms may have induced the changes of surfactant that we measured at one week after the initial transplantation injury in the present study.…”

Section: Discussionmentioning

confidence: 99%

“…The remainder of BALF was centrifuged overnight at 100,000 g, 4 o C, to concentrate the surfactant in a pellet (P3) for the determination of the phospholipid-composition. The phospholipids were separated by thin layer chromatography according to Touchstone and coworkers (20) with the use of their solvent E .The amount of SP-A was assessed in BALF with a sandwich ELISA method (21). The measured amounts of SP-A do represent endogenous SP-A of the lung transplants, since the surfactant used did not contain SP-A.…”

Section: Components Of Alveolar Surfactantmentioning

confidence: 99%

Surfactant treatment before reperfusion improves the immediate function of lung transplants in rats.

Erasmus¹,

Petersen²,

Hofstede³

et al. 1996

Am J Respir Crit Care Med

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An impaired function of alveolar surfactant can cause lung transplant dysfunction early after reperfusion. In this study it was investigated whether treatment with surfactant before reperfusion improves the immediate function of lung transplants and whether an improved transplant function was associated with an increase in alveolar surfactant components. Left lungs with 6-h (n = 8) or prolonged 20-h ischemia (n = 10) were transplanted syngeneically in rats. In both ischemia groups half of the lung transplants were treated with surfactant just before reperfusion. Lung function was measured during reperfusion for 1 h. Thereafter, the rats were killed and bronchoalveolar lavage was performed to measure alveolar surfactant components. We found that surfactant treatment improved the immediate function of lung transplants in parallel with a higher amount of total surfactant phospholipids, a higher percentage of the heavy subtype of surfactant, a normalized percentage of phosphatidylcholine, and a higher amount of endogenous surfactant protein A (SP-A). We conclude that surfactant treatment before reperfusion does improve the immediate lung transplant function in rats in association with an increase in alveolar surfactant components. More particularly, the amount of (endogenous) SP-A is thought to be crucial for the efficacy of surfactant treatment after lung transplantation.

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“…Previous studies have demonstrated that apoptosis is an important process in injured to the lung epithelium in paraquat (PQ) poisoning ( 1 , 2 ). The mechanisms of apoptosis are highly complex and involve oxidative/nitrative stress impairment to the function of mitochondria with the reduction of the mitochondrial membrane potential (ΔΨ), resulting in an increase of superoxide formation and reduced production of adenosine 5′-triphosphate (ATP) ( 3 , 4 ). Previous studies suggest that adenosine 5′-monophosphate-activated protein kinase (AMPK) is one of the most important molecules in the stimulation of ATP production and protection against oxidative/nitrative stress in mitochondria ( 5 , 6 ).…”

Section: Introductionmentioning

confidence: 99%

Adiponectin ameliorates the apoptotic effects of paraquat on alveolar type II cells via improvements in mitochondrial function

Zou

Zhou

et al. 2016

Molecular Medicine Reports

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Previous studies have demonstrated that excessive reactive oxygen/nitrogen species (ROS/RNS)-induced apoptosis is an important feature of the injury to the lung epithelium in paraquat (PQ) poisoning. However the precise mechanisms of PQ-induced dysfunction of the mitochondria, where ROS/RNS are predominantly produced, remain to be fully elucidated. Whether globular adiponectin (gAd), a potent molecule protective to mitochondria, regulates the mitochondrial function of alveolar type II cells to reduce PQ-induced ROS/RNS production remains to be investigated. The current study aimed to investigate the precise mechanisms of PQ poisoning in the mitochondria of alveolar type II cells, and to elucidate the role of gAd in protecting against PQ-induced lung epithelium injury. Therefore, lung epithelial injury was induced by PQ co-culture of alveolar type II A549 cells for 24 h. gAd was administrated to and removed from the injured cells in after 24 h. PQ was observed to reduce cell viability and increase apoptosis by ~1.5 fold in A549 cells. The oxidative/nitrative stress, resulting from ROS/RNS and disordered mitochondrial function were evidenced by increased normalO2−., NO production and reduced mitochondrial membrane potential (ΔΨ), adenosine 5′-triphosphate (ATP) content in PQ-poisoned A549 cells. gAd treatment significantly reversed the PQ-induced cell injury and mitochondrial dysfunction in A549 cells. The protective effects of gAd were partly abrogated by an adenosine 5′-monophosphate-activated protein kinase (AMPK) inhibitor, compound C. The results suggest that reduced ΔΨ and ATP content may result in PQ-induced mitochondrial dysfunction of the lung epithelium, which constitutes a novel mechanism for gAd exerting pulmonary protection against PQ poisoning via AMPK activation.

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Phospholipid synthesis in isolated alveolar type II cells exposed in vitro to paraquat and hyperoxia

Cited by 14 publications

References 25 publications

Effects of Early Surfactant Treatment Persisting for One Week after Lung Transplantation in Rats

Effects of Early Surfactant Treatment Persisting for One Week after Lung Transplantation in Rats

Surfactant treatment before reperfusion improves the immediate function of lung transplants in rats.

Adiponectin ameliorates the apoptotic effects of paraquat on alveolar type II cells via improvements in mitochondrial function

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