Sphingolipids in Lung Growth and Repair

Tibboel, Jeroen; Jongste, Johan C. de; Post, Martin

doi:10.1378/chest.13-0967

Cited by 46 publications

(47 citation statements)

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“…They have been identified as an important class of molecules involved in a variety of diseases, such as asthma (Lai et al, 2011), chronic obstructive pulmonary disease (Lahiri and Futerman, 2007), and rheumatoid arthritis (Kamada et al, 2009). Of recent interest is the role of sphingolipids in inflammation and inflammatory diseases, specifically in the lungs (Tibboel et al, 2014). In particular, sphingosine kinase (SK) and its product, sphingosine-1-phosphate (S1P), have been extensively implicated in these processes (Snider et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

A metabolomics approach to studying the effects of Jinxin oral liquid on RSV-infected mice using UPLC/LTQ-Orbitrap mass spectrometry

Xie

et al. 2015

Journal of Ethnopharmacology

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Section: Discussionmentioning

confidence: 99%

A metabolomics approach to studying the effects of Jinxin oral liquid on RSV-infected mice using UPLC/LTQ-Orbitrap mass spectrometry

Xie

et al. 2015

Journal of Ethnopharmacology

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“…It has been associated with increased lung infections and Brought to you by | New York University Bobst Library Technical Services Authenticated Download Date | 5/27/15 8:12 AM inflammation, and also may lead to apoptotic death of lung cells (Tibboel et al, 2014). The origin of increased ceramide in CF has been associated with increased sphingomyelinase activity and/or de novo ceramide synthesis, and can be detected in CF lung biopsy tissue, cultured cells and/or broncholavage fluid and cells.…”

Section: Other Potential Uses For Acid Ceramidasementioning

confidence: 99%

The molecular medicine of acid ceramidase

Frohbergh

Schuchman

2015

Biological Chemistry

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Acid ceramidase (N-acylsphingosine deacylase, EC 3.5.1.23; AC) is the lipid hydrolase responsible for the degradation of ceramide into sphingosine and free fatty acids within lysosomes. The enzymatic activity was first identified over four decades ago and is deficient in two rare inherited disorders, Farber lipogranulomatosis (Farber disease) and spinal muscular atrophy with myoclonic epilepsy (SMA-PME). Importantly, AC not only hydrolyzes ceramide into sphingosine within acidic compartments, but also can synthesize ceramide from sphingosine at neutral pH, suggesting that the enzyme may have diverse functions depending on its subcellular location and the local pH. Within cells, AC exists in a complex with other lipid hydrolases and requires a polypeptide cofactor (saposin D) for full hydrolytic activity. Recent studies also have shown that AC is overexpressed in several human cancers, and that inhibition of this enzyme may be a useful cancer drug target. Aberrant AC activity has also been described in several other common diseases. The cDNA and gene (ASAH1) encoding AC have been isolated, several mouse models of AC deficiency have been constructed, and the recombinant enzyme is currently being manufactured for the treatment of Farber disease and SMA-PME. Current information concerning the biology of this enzyme and its role in human disease is reviewed within.

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“…Ceramide (Cer), a sphingolipid metabolite, induces the apoptosis of alveolar epithelial cells and the formation of the alveolus, while sphingosine-1-phosphate (S1P) maintains the survival of cells, which are important for the structural and functional development of the lung [15]. The imbalance of Cer and S1P leads to alveolar enlargement or fibrosis and is involved in the onset of COPD, asthma, lung fibrosis and lung cancer [16]. Although a phospholipid metabolism profile of pulmonary tissue after PM 2.5 exposure has been carried out [17], the global lipid metabolism change induced by PM 2.5 is largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Metabolomics analysis reveals that benzo[a]pyrene, a component of PM2.5, promotes pulmonary injury by modifying lipid metabolism in a phospholipase A2-dependent manner in vivo and in vitro

et al. 2017

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Particulate matter with an aerodynamic diameter less than 2.5 μM (PM2.5) is one of the major environmental pollutants in China. In this study, we carried out a metabolomics profile study on PM2.5-induced inflammation. PM2.5 from Beijing, China, was collected and given to rats through intra-tracheal instillation in vivo. Acute pulmonary injury were observed by pulmonary function assessment and H.E. staining. The lipid metabolic profile was also altered with increased phospholipid and sphingolipid metabolites in broncho-alveolar lavage fluid (BALF) after PM2.5 instillation. Organic component analysis revealed that benzo[a]pyrene (BaP) is one of the most abundant and toxic components in the PM2.5 collected on the fiber filter. In vitro, BaP was used to treat A549 cells, an alveolar type II cell line. BaP (4 μM, 24 h) induced inflammation in the cells. Metabolomics analysis revealed that BaP (4 μM, 6 h) treatment altered the cellular lipid metabolic profile with increased phospholipid metabolites and reduced sphingolipid metabolites and free fatty acids (FFAs). The proportion of ω–3 polyunsaturated fatty acid (PUFA) was also decreased. Mechanically, BaP (4 μM) increased the phospholipase A2 (PLA2) activity at 4 h as well as the mRNA level of Pla2g2a at 12 h. The pro-inflammatory effect of BaP was reversed by the cytosolic PLA2 (cPLA2) inhibitor and chelator of intracellular Ca2+. This study revealed that BaP, as a component of PM2.5, induces pulmonary injury by activating PLA2 and elevating lysophosphatidylcholine (LPC) in a Ca2+-dependent manner in the alveolar type II cells.

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Sphingolipids in Lung Growth and Repair

Cited by 46 publications

References 98 publications

A metabolomics approach to studying the effects of Jinxin oral liquid on RSV-infected mice using UPLC/LTQ-Orbitrap mass spectrometry

A metabolomics approach to studying the effects of Jinxin oral liquid on RSV-infected mice using UPLC/LTQ-Orbitrap mass spectrometry

The molecular medicine of acid ceramidase

Metabolomics analysis reveals that benzo[a]pyrene, a component of PM2.5, promotes pulmonary injury by modifying lipid metabolism in a phospholipase A2-dependent manner in vivo and in vitro

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