Secretory phospholipases A2 in inflammatory and allergic diseases: Not just enzymes

Triggiani, Massimo; Granata, Francescopaolo; Giannattasio, Giorgio; Marone, Gianni

doi:10.1016/j.jaci.2005.08.011

Cited by 110 publications

(122 citation statements)

References 54 publications

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“…These higher levels were associated with greater levels of eicosanoids and Th2 cytokines in BALF from PLA 2 R 2/2 mice than from PLA 2 R +/+ mice. Previous animal and human studies showed that sPLA 2 have an important role in the genesis of airway inflammation through the production of proinflammatory eicosanoids in a variety of inflammatory cells (11)(12)(13)(14)(15). Eicosanoids including CysLTs, LTB 4 , and PGD 2 cause lung inflammation directly or indirectly through induction of Th2 cytokines (1)(2)(3)(4).…”

Section: Discussionmentioning

confidence: 99%

“…Previous reports raised the possibility that the cytoplasmic tail of PLA 2 R is directly linked to a signal transduction system that induces cell proliferation, eicosanoid production, and inflammation independent of intrinsic enzymatic activities of sPLA 2 (15,33,34). We and others showed that some sPLA 2 act in concert with cPLA 2 a to induce eicosanoid generation (35,36), and PLA 2 R-mediated intracellular transduction signals can participate in the cross talk between sPLA 2 -IB and cPLA 2 a (37).…”

Section: Discussionmentioning

confidence: 99%

“…These eicosanoids are 5-lipoxygenase and cyclooxygenase metabolites of arachidonic acids, and the cellular availability of arachidonic acid is tightly controlled by hydrolysis of membrane phospholipids via the catalytic activity of phospholipases A 2 (PLA 2 ) (5-10). Previous animal and human studies showed that PLA 2 is involved in the genesis of airway inflammation through proinflammatory eicosanoids (11)(12)(13)(14)(15).…”

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confidence: 99%

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Deficiency of Phospholipase A2 Receptor Exacerbates Ovalbumin-Induced Lung Inflammation

Tamaru

Mishina

Watanabe

et al. 2013

The Journal of Immunology

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Secretory phospholipase A2 (sPLA2) plays a critical role in the genesis of lung inflammation through proinflammatory eicosanoids. A previous in vitro experiment showed a possible role of cell surface receptor for sPLA2 (PLA2R) in the clearance of extracellular sPLA2. PLA2R and groups IB and X sPLA2 are expressed in the lung. This study examined a pathogenic role of PLA2R in airway inflammation using PLA2R-deficient (PLA2R−/−) mice. Airway inflammation was induced by immunosensitization with OVA. Compared with wild-type (PLA2R+/+) mice, PLA2R−/− mice had a significantly greater infiltration of inflammatory cells around the airways, higher levels of groups IB and X sPLA2, eicosanoids, and Th2 cytokines, and higher numbers of eosinophils and neutrophils in bronchoalveolar lavage fluid after OVA treatment. In PLA2R−/− mice, intratracheally instilled [125I]-labeled sPLA2-IB was cleared much more slowly from bronchoalveolar lavage fluid compared with PLA2R+/+ mice. The degradation of the instilled [125I]-labeled sPLA2-IB, as assessed by trichloroacetic acid-soluble radioactivity in bronchoalveolar lavage fluid after instillation, was lower in PLA2R−/− mice than in PLA2R+/+ mice. In conclusion, PLA2R deficiency increased sPLA2-IB and -X levels in the lung through their impaired clearance from the lung, leading to exaggeration of lung inflammation induced by OVA treatment in a murine model.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Deficiency of Phospholipase A2 Receptor Exacerbates Ovalbumin-Induced Lung Inflammation

Tamaru

Mishina

Watanabe

et al. 2013

The Journal of Immunology

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“…13 Several sPLA 2 isoforms are expressed and released by infl ammatory cells. 19 In addition to infl ammatory cells, the epithelial cells lining the respiratory tract may be an important source of sPLA 2 . 6,9,20-22 It has not been shown which airway epithelial cells produce sPLA 2 , or which cells types respond to sPLA 2 by producing leukotrienes.…”

Section: [ 1 4 7 # 6 C H E S T J U N E 2 0 1 5 ]mentioning

confidence: 99%

Secretory Phospholipases A 2 Are Secreted From Ciliated Cells and Increase Mucin and Eicosanoid Secretion From Goblet Cells

Tanabe

Shimokawaji

Kanoh

et al. 2015

Chest

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BACKGROUND: Secretory phospholipases A 2 (sPLA 2 ) initiate the biosynthesis of eicosanoids, are increased in the airways of people with severe asthma, and induce mucin hypersecretion. We used IL-13-transformed, highly enriched goblet cells and differentiated (ciliary cellenriched) human bronchial epithelial cell culture to evaluate the relative contribution of ciliated and goblet cells to airway sPLA 2 generation and response. We wished to determine the primary source(s) of sPLA 2 and leukotrienes in human airway epithelial cells.

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“…phospholipases A2 (plA2s) are phospholipid hydrolase enzymes that mediate the release of biologically active fatty acids and lysophospholipids such as arachidonic acid (AA) and lysophosphatidylcholine, which are the precursors of eicosanoids and platelet-activating factor, respectively (9,10). It was reported that secretory phospholipase A2-IIa (splA2-IIa) is overexpressed in almost all human prostate cancer specimens and elevated levels correlate with tumor grade (11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

Vav3 oncogene is involved in regulation of secretory phospholipase A2-IIa expression in prostate cancer

Dong

Liu²,

Levin³

et al. 2011

Oncol Rep

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Abstract. our previous study revealed that Vav3 oncogene and secretory phospholipase A2-IIa (splA2-IIa) are overexpressed in androgen-independent prostate cancer cells relative to their androgen-dependent counterparts and contribute to development of hormone refractory prostate cancer. Vav3 is a multiple function protein with both signaling molecule and coactivator activities. splA2-IIa is a downstream effector of Her/Her2-pI3K-Akt-nF-κB signaling and involved in inflammatory response and tumorigenesis. The aim of the current study was to determine whether Vav3 is involved in up-regulation of splA2-IIa expression, given that Vav3 signals in the Her/Her2-elicited pathway. Among 46 prostate cancer specimens examined, Vav3 and splA2-IIa are overexpressed in 48 and 83% human prostate cancers, respectively. Vav3 overexpression is significantly associated with a high level expression of sPLA2-IIa. In addition, significant Vav3 nuclear localization is observed in two prostate cancer specimens, supporting a coactivator activity in prostate cancer cells. Further analysis revealed that Vav3 up-regulates expression of the splA2-IIa gene at the transcriptional level via Her/Her2-pI3K-Akt-nF-κB signaling. these data revealed that Vav3 overexpression as an additional underlying mechanism contributes to elevated splA2-IIa expression in prostate cancer.

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Secretory phospholipases A2 in inflammatory and allergic diseases: Not just enzymes

Cited by 110 publications

References 54 publications

Deficiency of Phospholipase A2 Receptor Exacerbates Ovalbumin-Induced Lung Inflammation

Deficiency of Phospholipase A2 Receptor Exacerbates Ovalbumin-Induced Lung Inflammation

Secretory Phospholipases A 2 Are Secreted From Ciliated Cells and Increase Mucin and Eicosanoid Secretion From Goblet Cells

Vav3 oncogene is involved in regulation of secretory phospholipase A2-IIa expression in prostate cancer

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