Synthesis of phosphatidylcholine in rats with oleic acid-induced pulmonary edema and effect of exogenous pulmonary surfactant on its De Novo synthesis

Gao, Xiwen; Qian, Peng; Cen, Dong; Hong, Weijun; Peng, Qing; Xue, Min

doi:10.1371/journal.pone.0193719

Cited by 8 publications

(7 citation statements)

References 23 publications

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“…Pathway assessments demonstrated that with the suppression of background noise and subsequent screening of variants highly enriched in the GP7 case, we observed some novel pathways that previously weren't recognized as statistically signi cant for ARDS such as C-C chemokine receptor type 3 (CCR3) signaling, phosphoribosyl pyrophosphate (PRPP) biosynthesis, inhibition of matrix metalloproteases, choline degradation, glutamine biosynthesis, actin cytoskeleton signaling and epithelial junction signaling. These molecules have documented roles in lung pathogenesis and physiological signaling [24,27,[43][44][45]. This indicates that there are potentially several signaling molecules derived from GP7 that could be prevalent due to the disease process.…”

Section: Discussionmentioning

confidence: 99%

Characterizing a Focused Landscape of Familial Acute Respiratory Distress Syndrome

2020

Biomark Applic

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Background Acute respiratory distress syndrome (ARDS) affects approximately 190,600 patients per year in the United States, with mortality up to 45%. ARDS can occur as primary disease due to various factors (e.g. bacterial or viral pneumonia, gastric aspiration, lung contusion, toxic inhalation, and near drowning) or as secondary disease due to sepsis, pancreatitis, severe trauma, massive blood transfusion, and burn.We hypothesized that ARDS-affected individuals have patterns of variants in their physiological repertoire that can be tracked and utilized to complement clinical diagnosis and/or clinical monitoring. MethodsThe goals of this study were to: (1) characterize the landscape of variants within protein coding but we also studied UTR regions in ARDS using an Exome sequencing approach; (2), determine the variations in signaling pathways across ARDS; and (3) use computational approaches to explore the functional consequences of ARDS. Towards this we assessed an ARDS-affected individual in the context of unaffected individuals from the same family as well as unrelated ARDS cases, in order to elucidate underlying inheritance patterns of "private variants". Private variants consist of variants shared by ARDS cases but not found in unaffected individuals. Results Whole exome sequencing yielded 3,516 variants represented by 2,354 genes. Of these, 128 variants were shared across all ARDS cases. Of these, there were 24 unique variants represented by 9 ARDS genes shared by the primary ARDS-case and unrelated individuals with ARDS. The overall genes identi ed and subsequent analysis, demonstrate that there are important biological pathways that distinguish ARDS cases from or from non-ARDS. These pathways include: cell-to-cell signaling interaction, cell growth and proliferation and cell morphology. The data also show a coordinated effort amongst biological processes such as liver hyperproliferation and cell death that underlie the pathogenesis of ARDS. Conclusions These in-silico discoveries demonstrate a role for private variants shared by ARDS cases to be leveraged as biomarkers for clinical diagnosis and/or monitoring of ARDS.

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Section: Discussionmentioning

confidence: 99%

Characterizing a Focused Landscape of Familial Acute Respiratory Distress Syndrome

2020

Biomark Applic

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“…In an effort to characterize variant patterns across all ARDS cases from this study, we parsed out the group Pathway assessments demonstrated that with the suppression of background noise and subsequent screening of variants highly enriched in the GP7 case, we observed some novel pathways that previously weren't recognized as statistically significant for ARDS such as C-C chemokine receptor type 3 (CCR3) signaling, phosphoribosyl pyrophosphate (PRPP) biosynthesis, inhibition of matrix metalloproteases, choline degradation, glutamine biosynthesis, actin cytoskeleton signaling and epithelial junction signaling. These molecules have documented roles in lung pathogenesis and physiological signaling [24,27,[43][44][45]. This indicates that there are potentially several signaling molecules derived from GP7 that could be prevalent due to the disease process.…”

Section: Discussionmentioning

confidence: 99%

Characterizing a focused landscape of familial acute respiratory distress syndrome

Toby¹,

Thomas²,

Thorenoor³

et al. 2019

Preprint

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Background Acute respiratory distress syndrome (ARDS) affects approximately 190,600 patients per year in the United States, with mortality up to 45%. ARDS can occur as primary disease due to various factors (e.g. bacterial or viral pneumonia, gastric aspiration, lung contusion, toxic inhalation, and near drowning) or as secondary disease due to sepsis, pancreatitis, severe trauma, massive blood transfusion, and burn. We hypothesized that ARDS-affected individuals have patterns of variants in their physiological repertoire that can be tracked and utilized to complement clinical diagnosis and/or clinical monitoring. Methods The goals of this study were to: (1) characterize the landscape of variants within protein coding but we also studied UTR regions in ARDS using an Exome sequencing approach; (2), determine the variations in signaling pathways across ARDS; and (3) use computational approaches to explore the functional consequences of ARDS. Towards this we assessed an ARDS-affected individual in the context of unaffected individuals from the same family as well as unrelated ARDS cases, in order to elucidate underlying inheritance patterns of “private variants”. Private variants consist of variants shared by ARDS cases but not found in unaffected individuals. Results Whole exome sequencing yielded 3,516 variants represented by 2,354 genes. Of these, 128 variants were shared across all ARDS cases. Of these, there were 24 unique variants represented by 9 ARDS genes shared by the primary ARDS-case and unrelated individuals with ARDS. The overall genes identified and subsequent analysis, demonstrate that there are important biological pathways that distinguish ARDS cases from or from non-ARDS. These pathways include: cell-to-cell signaling interaction, cell growth and proliferation and cell morphology. The data also show a coordinated effort amongst biological processes such as liver hyperproliferation and cell death that underlie the pathogenesis of ARDS. Conclusions These in-silico discoveries demonstrate a role for private variants shared by ARDS cases to be leveraged as biomarkers for clinical diagnosis and/or monitoring of ARDS.

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“…Lipid accumulation and oxidation is essential to atherosclerosis pathogenesis to trigger inflammation and macrophage recruitment in the plaques. Activated macrophages need choline for the synthesis of phosphatidylcholine [ 102 ], a major phospholipid acting as a structural building block of biological membranes and as a second messenger implicated in cell surface receptors regulation [ 103 ]. Choline is taken up by specific transporter then metabolized by choline kinase to be finally incorporated in a cell’s membrane [ 104 , 105 ].…”

Section: Clinical Findings Of Nuclear Medicine To Identify and Stratify Vascular Inflammationmentioning

confidence: 99%

Advances in Radiopharmaceutical Sciences for Vascular Inflammation Imaging: Focus on Clinical Applications

Prigent

Vigne

2021

Molecules

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Biomedical imaging technologies offer identification of several anatomic and molecular features of disease pathogenesis. Molecular imaging techniques to assess cellular processes in vivo have been useful in advancing our understanding of several vascular inflammatory diseases. For the non-invasive molecular imaging of vascular inflammation, nuclear medicine constitutes one of the best imaging modalities, thanks to its high sensitivity for the detection of probes in tissues. 2-[18F]fluoro-2-deoxy-d-glucose ([18F]FDG) is currently the most widely used radiopharmaceutical for molecular imaging of vascular inflammatory diseases such as atherosclerosis and large-vessel vasculitis. The combination of [18F]FDG and positron emission tomography (PET) imaging has become a powerful tool to identify and monitor non-invasively inflammatory activities over time but suffers from several limitations including a lack of specificity and avid background in different localizations. The use of novel radiotracers may help to better understand the underlying pathophysiological processes and overcome some limitations of [18F]FDG PET for the imaging of vascular inflammation. This review examines how [18F]FDG PET has given us deeper insight into the role of inflammation in different vascular pathologies progression and discusses perspectives for alternative radiopharmaceuticals that could provide a more specific and simple identification of pathologies where vascular inflammation is implicated. Use of these novel PET tracers could lead to a better understanding of underlying disease mechanisms and help inform the identification and stratification of patients for newly emerging immune-modulatory therapies. Future research is needed to realize the true clinical translational value of PET imaging in vascular inflammatory diseases.

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Synthesis of phosphatidylcholine in rats with oleic acid-induced pulmonary edema and effect of exogenous pulmonary surfactant on its De Novo synthesis

Cited by 8 publications

References 23 publications

Characterizing a Focused Landscape of Familial Acute Respiratory Distress Syndrome

Characterizing a Focused Landscape of Familial Acute Respiratory Distress Syndrome

Characterizing a focused landscape of familial acute respiratory distress syndrome

Advances in Radiopharmaceutical Sciences for Vascular Inflammation Imaging: Focus on Clinical Applications

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