Surfactant protein B inhibits secretory phospholipase A<sub>2</sub>hydrolysis of surfactant phospholipids

Hite, R. Duncan; Grier, Bonnie L.; Waite, B. Moseley; Veldhuizen, Ruud A. W.; Possmayer, Fred; Yao, Li–Juan; Seeds, Michael C.

doi:10.1152/ajplung.00054.2011

Cited by 27 publications

(22 citation statements)

References 55 publications

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“…sPLA 2 (IIA) is secreted by lung mast cells and macrophages and increased levels of this enzyme have been detected in BAL fluid of subjects with pneumonia, sarcoidosis, and ARDS (12,20,27,35). Our results also suggest that sPLA 2 (IIA) may also be secreted by HASM.…”

Section: Discussionsupporting

confidence: 66%

IL-6 trans-signaling increases expression of airways disease genes in airway smooth muscle

Robinson

Deshpande

Chou

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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Section: Discussionsupporting

confidence: 66%

IL-6 trans-signaling increases expression of airways disease genes in airway smooth muscle

Robinson

Deshpande

Chou

et al. 2015

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…A likely underlying reason is the heterogeneity of the disease, which might be associated with a direct insult by, e.g., infection, aspiration, or injurious ventilation, or an indirect one during situations of severe systemic inflammation, or, frequently, a combination thereof. Efforts to define endogenous pathways or molecules that protect from ALI have recently significantly contributed to our understanding of ALI pathophysiology (5,36,51,81,95,99,132,150,176,189,226,245,254,256,261). Imai et al (106) were the first to suggest that the signals impacting on the balance between angiotensin converting enzymes (ACE) 1 and 2 modulate the degree of inflammatory lung injury after sepsis, and ACE I/D polymorphism was recently associated with mortality risk of ALI/ ARDS in patients (152).…”

Section: Putative Candidates For Treatment Of Alimentioning

confidence: 99%

Novel concepts of acute lung injury and alveolar-capillary barrier dysfunction

Herold

Gabrielli

Vadász

2013

American Journal of Physiology-Lung Cellular and Molecular Phys

183

178

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Herold S, Gabrielli NM, Vadász I. Novel concepts of acute lung injury and alveolar-capillary barrier dysfunction. Am J Physiol Lung Cell Mol Physiol 305: L665-L681, 2013. First published September 13, 2013 doi:10.1152/ajplung.00232.2013In this review we summarize recent major advances in our understanding on the molecular mechanisms, mediators, and biomarkers of acute lung injury (ALI) and alveolar-capillary barrier dysfunction, highlighting the role of immune cells, inflammatory and noninflammatory signaling events, mechanical noxae, and the affected cellular and molecular entities and functions. Furthermore, we address novel aspects of resolution and repair of ALI, as well as putative candidates for treatment of ALI, including pharmacological and cellular therapeutic means. alveolar-capillary barrier dysfunction; molecular mechanism; pharmacological and cell-based therapy; pulmonary edema; zaacute lung injury/acute respiratory distress syndrome Immune Cells and Inflammatory Signaling Pathways in ALIOne of the central concepts in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) is that an unbalanced quantity or quality of the inflammatory response aggravates epithelial or endothelial injury. This includes a dysregulated recruitment of leukocytes and/or an exaggerated activation of these cells; inappropriate expression of cytokines, lipid mediators, or reactive oxygen species; enhanced activation of death receptor signaling (97,98,140,207,240); or an uncontrolled activity of platelets or the coagulation cascade (154). In general, these responses are initiated and maintained by recognition of danger-or pathogen-associated molecular patterns

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“…Therefore, many pharmacological studies covering inhibitors to prevent AA production have been performed in various cancer types [22]. Notably, SP-B was reported to inhibit the activity of sPLA 2 [23]. Although the mechanism is elusive, it can be assumed that SP-B is involved in sPLA 2 -induced tumor progression.…”

mentioning

confidence: 99%

Surfactant Protein B Suppresses Lung Cancer Progression by Inhibiting Secretory Phospholipase A2 Activity and Arachidonic Acid Production

Lee

Kim

Kang

et al. 2017

Cell Physiol Biochem

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Background/Aims: Radiotherapy is applied to patients with inoperable cancer types including advanced stage non-small cell lung cancer (NSCLC) and radioresistance functions as a critical obstacle in radiotherapy. This study was aimed to investigate the mechanism of radioresistance regulated by surfactant protein B (SP-B). Methods: To investigate the role of SP-B in radioresistance, ΔSFTPB A549 cell line was established and SP-B expression was analyzed. In response to ionizing radiation (IR), the change of SP-B expression was analyzed in A549 and NCI-H441 cell lines. Conditioned media (CM) from NSCLC cells were utilized to evaluate the downstream signaling pathway. The in vivo effects of SP-B were assessed through mouse xenograft model with intratumoral injection of CM. Results: In response to IR, NSCLC cell lines showed decreased SP-B regulated by the TGF-β signaling and decreased SP-B stimulated cell survival and epithelial-mesenchymal transition. Treatment with CM from irradiated cells activated sPLA 2 , enhanced protein kinase Cδ-MAPKs signaling pathway, and increased arachidonic acid production. We confirmed the in vivo roles of SP-B through mouse xenograft model. Conclusion: Our results revealed that down-regulation of SP-B was involved in the radiation-induced metastatic conversion of NSCLC and provided evidence that SP-B acted as a suppressor of NSCLC progression.S. Lee and D. Kim contributed equally to this work.

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Surfactant protein B inhibits secretory phospholipase A₂hydrolysis of surfactant phospholipids

Abstract: Seeds MC. Surfactant protein B inhibits secretory phospholipase A 2 hydrolysis of surfactant phospholipids.

Cited by 27 publications

References 55 publications

IL-6 trans-signaling increases expression of airways disease genes in airway smooth muscle

IL-6 trans-signaling increases expression of airways disease genes in airway smooth muscle

Novel concepts of acute lung injury and alveolar-capillary barrier dysfunction

Surfactant Protein B Suppresses Lung Cancer Progression by Inhibiting Secretory Phospholipase A2 Activity and Arachidonic Acid Production

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Surfactant protein B inhibits secretory phospholipase A2hydrolysis of surfactant phospholipids

Abstract: Seeds MC. Surfactant protein B inhibits secretory phospholipase A 2 hydrolysis of surfactant phospholipids.

Cited by 27 publications

References 55 publications

IL-6 trans-signaling increases expression of airways disease genes in airway smooth muscle

IL-6 trans-signaling increases expression of airways disease genes in airway smooth muscle

Novel concepts of acute lung injury and alveolar-capillary barrier dysfunction

Surfactant Protein B Suppresses Lung Cancer Progression by Inhibiting Secretory Phospholipase A2 Activity and Arachidonic Acid Production

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Surfactant protein B inhibits secretory phospholipase A₂hydrolysis of surfactant phospholipids