Involvement of Vitronectin in Lipopolysaccaride-Induced Acute Lung Injury

Tsuruta, Yuko; Park, Young-Jun; Siegal, Gene P.; Liu, Gang; Abraham, Edward

doi:10.4049/jimmunol.179.10.7079

Cited by 63 publications

(81 citation statements)

References 46 publications

(48 reference statements)

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“…The murine ALI model was used as previously described (28,29). Briefly, mice were anesthetized with isoflurane.…”

Section: In Vivo Ali Modelmentioning

confidence: 99%

“…Mouse neutrophils were purified from bone marrow cell suspensions as described previously (28,29). Briefly, the femur and tibia of a mouse were Ϫ/Ϫ inflammatory cells.…”

Section: Isolation Of Neutrophilsmentioning

confidence: 99%

“…MPO was measured using a modification of a previously described method (28,29). In brief, lung tissue was homogenized using a Glas-Col homogenizer in 0.5 ml of 0.5% hexadecyltrimethyl ammonium bromide in 50 mM potassium phosphate buffer (pH 6.0).…”

Section: Myeloperoxidase (Mpo) Assaymentioning

confidence: 99%

“…Nuclear extracts were prepared and assayed by EMSA as previously described (28). For analysis of NF-B, the B DNA sequence of the Ig gene was used.…”

Section: Emsamentioning

confidence: 99%

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p53 Attenuates Lipopolysaccharide-Induced NF-κB Activation and Acute Lung Injury

Liu

Park

Tsuruta

et al. 2009

The Journal of Immunology

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124

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The transcriptional factor p53 has primarily been characterized for its central role in the regulation of oncogenesis. A reciprocal relationship between the activities of p53 and NF-B has been demonstrated in cancer cells, but there is little information concerning interactions between p53 and NF-B in inflammatory processes. In this study, we found that neutrophils and macrophages lacking p53, i.e., p53

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“…The murine ALI model was used as previously described (28,29). Briefly, mice were anesthetized with isoflurane.…”

Section: In Vivo Ali Modelmentioning

confidence: 99%

“…Mouse neutrophils were purified from bone marrow cell suspensions as described previously (28,29). Briefly, the femur and tibia of a mouse were Ϫ/Ϫ inflammatory cells.…”

Section: Isolation Of Neutrophilsmentioning

confidence: 99%

Section: Myeloperoxidase (Mpo) Assaymentioning

confidence: 99%

“…Nuclear extracts were prepared and assayed by EMSA as previously described (28). For analysis of NF-B, the B DNA sequence of the Ig gene was used.…”

Section: Emsamentioning

confidence: 99%

See 2 more Smart Citations

p53 Attenuates Lipopolysaccharide-Induced NF-κB Activation and Acute Lung Injury

Liu

Park

Tsuruta

et al. 2009

The Journal of Immunology

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124

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“…Tissue levels of vitronectin markedly increase in pathophysiologic settings associated with acute inflammation, such as severe sepsis, and appear to contribute to organ injury in such conditions (7,8). Vitronectin promotes neutrophil adhesion and migration through interaction with integrins, including a v b 3 , and other ligands, such as the urokinase plasminogen activator (uPA) receptor (uPAR) (9, 10).…”

mentioning

confidence: 99%

Vitronectin Inhibits Neutrophil Apoptosis through Activation of Integrin-Associated Signaling Pathways

Bae

Żmijewski²,

Deshane

et al. 2012

Am J Respir Cell Mol Biol

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Vitronectin is present in large concentrations in serum and the extracellular matrix. Although vitronectin is known to modulate neutrophil adhesion and chemotaxis, and to contribute to neutrophil-associated proinflammatory processes, a role in apoptosis has not been demonstrated. In the present studies, we found that neutrophils demonstrated more rapid progression to spontaneous or TNF-related apoptosisinducing ligand-induced apoptosis when incubated under vitronectinfree conditions than when vitronectin was present. The ability of native vitronectin to delay neutrophil apoptosis was not recapitulated by the vitronectin somatomedin B domain. In contrast, inclusion of the cyclo[Arg-Gly-Asp-D-Phe-Val] peptide in cultures containing vitronectin resulted in enhanced neutrophil apoptosis, showing that the vitronectin RGD motif (Arg-Gly-Asp motif) was responsible for the antiapoptotic effects of vitronectin. Addition of antibodies to b 1 , b 3 , or b 5 , but not to b 2 or b 4 integrins, reversed the ability of vitronectin to diminish neutrophil apoptosis. The ability of vitronectin to enhance neutrophil viability was dependent on activation of phosphatidylinositol 3-kinase and extracellular signal-regulated kinase 1/2 kinases, but not on the p38 kinase. Increased numbers of apoptotic neutrophils were present in the lungs of LPS-treated transgenic vitronectin-deficient mice, as compared with control mice. These results demonstrate a novel antiapoptotic function for vitronectin.Keywords: vitronectin; inflammation; neutrophils; apoptosis; lung injury Although neutrophils play a central role in host defense against invading microbes, organ injury can result if neutrophils activated to produce proinflammatory mediators remain in tissues for prolonged periods. The timely progression of neutrophils to apoptotic cell death and subsequent clearance is essential for the successful resolution of neutrophil-associated inflammatory processes (1). Under normal conditions, neutrophils are short lived, but during inflammatory responses, such as acute lung injury, they demonstrate prolonged viability. The importance of diminished neutrophil apoptosis in promoting tissue injury during inflammatory processes has been demonstrated by studies in which pharmacologically induced increase in apoptosis resulted in diminished severity of organ dysfunction, such as lung injury induced by LPS or hemorrhage (2-4).Vitronectin is a glycoprotein present in large concentrations in serum, extracellular matrix, and platelets, and participates in the regulation of coagulation, fibrinolysis, and complement activation (5, 6). Tissue levels of vitronectin markedly increase in pathophysiologic settings associated with acute inflammation, such as severe sepsis, and appear to contribute to organ injury in such conditions (7,8). Vitronectin promotes neutrophil adhesion and migration through interaction with integrins, including a v b 3 , and other ligands, such as the urokinase plasminogen activator (uPA) receptor (uPAR) (9, 10). The first 43 amino acids of N-...

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Laurus nobilis leaf extract controls inflammation by suppressing NLRP3 inflammasome activation

Lee

Shin

Kim

et al. 2018

Journal Cellular Physiology

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Laurus nobilis Linn. (Lauraceae), commonly known as Bay, has been used as a traditional medicine in the Mediterranean and Europe to treat diverse immunological disorders. Although the effects of L. nobilis on immunosuppression have been reported, the detailed underlying mechanism remains unclear. In this study, to elucidate the anti‐inflammatory mechanism of L. nobilis, we examined the effect of L. nobilis leaf extract on inflammasome activation in mouse bone marrow‐derived macrophages. L. nobilis leaf extract inhibited NOD‐like receptor pyrin domain‐containing 3 (NLRP3) inflammasome activation, which was associated with caspase‐1 activation, interleukin‐1β secretion, and apoptosis‐associated speck‐like protein containing a CARD (ASC) pyroptosome complex formation. We also observed that 1,8‐cineole, the major component of L. nobilis extract, consistently suppressed NLRP3 inflammasome activation. Furthermore, L. nobilis leaf extract attenuated the in vivo expression of proinflammatory cytokines in an acute lung injury mouse model. Our results provide the first evidence that L. nobilis leaf extract modulates inflammatory signaling by suppressing inflammasome activation.

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Involvement of Vitronectin in Lipopolysaccaride-Induced Acute Lung Injury

Cited by 63 publications

References 46 publications

p53 Attenuates Lipopolysaccharide-Induced NF-κB Activation and Acute Lung Injury

p53 Attenuates Lipopolysaccharide-Induced NF-κB Activation and Acute Lung Injury

Vitronectin Inhibits Neutrophil Apoptosis through Activation of Integrin-Associated Signaling Pathways

Laurus nobilis leaf extract controls inflammation by suppressing NLRP3 inflammasome activation

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