Involvement of the Receptor for Formylated Peptides in the in Vivo Anti-Migratory Actions of Annexin 1 and its Mimetics

Perretti, Mauro; Getting, Stephen J.; Solito, Egle; Murphy, Philip M.; Gao, Ji-Liang

doi:10.1016/s0002-9440(10)64667-6

Cited by 112 publications

(105 citation statements)

References 34 publications

(38 reference statements)

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“…Recently, the inhibitory effect of N-terminal Anx A1 peptides as well as the full-length Anx A1 was reported to be based on interaction with FPR1 as well as FPRL1 (FPR2). 15,16 Anx A1 was also reported to chemoattract certain tumor cells and its overexpression in head and neck squamous cell carcinoma, 17 pancreatic cancer, 18,19 and melanoma 20 was associated with increased tumor invasiveness and metastasis. Small interfering RNA-mediated knockdown of Anx A1 expression resulted in significant reduction of SKCO-15 colorectal adenocarcinoma cell invasion.…”

Section: Discussionmentioning

confidence: 99%

Annexin 1 Released by Necrotic Human Glioblastoma Cells Stimulates Tumor Cell Growth through the Formyl Peptide Receptor 1

Yang

Liu

Yao

et al. 2011

The American Journal of Pathology

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Highly malignant human gliomas overexpress the Gprotein-coupled chemoattractant receptor formyl peptide receptor (FPR1), which promotes tumor progression when activated. Our previous studies demonstrated that necrotic glioblastoma cells release chemotactic agonist(s) that activate FPR1 on viable tumor cells. In the present study, we identified an FPR1 agonist released by necrotic human glioblastoma cells.

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Section: Discussionmentioning

confidence: 99%

Annexin 1 Released by Necrotic Human Glioblastoma Cells Stimulates Tumor Cell Growth through the Formyl Peptide Receptor 1

Yang

Liu

Yao

et al. 2011

The American Journal of Pathology

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“…AnxA1 is relocalized from the cytoplasm to the plasma membrane in response to a variety of agonists including GCs, and can be externalized or secreted via an uncharacterized mechanism. The N-terminus of AnxA1, which is distinct from those of other annexins, is thought to exert anti-inflammatory effects by signalling through members of the formyl peptide receptor (FPR) family, in particular FPRL1 (Ernst et al, 2004;Gavins et al, 2003;Hayhoe et al, 2006;John et al, 2007;Perretti et al, 2001;Walther et al, 2000). This cell surface receptor also recognizes as a ligand lipoxin A 4 , a prostanoid involved in the resolution of inflammation.…”

Section: Annexin A1mentioning

confidence: 99%

Anti-inflammatory functions of glucocorticoid-induced genes

Clark

2007

Molecular and Cellular Endocrinology

237

193

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“…10 min before reperfusion. 2) To prevent the action of LXA 4 and ANXA-1, mice were treated with the ALX antagonist BOC-1 (2.0 mg/kg) (20), the 5-lipoxygenase inhibitor ZM230487 (5 mg/kg) (21) or the BLT 1/2 antagonist CP-105696 (3 mg/kg) (22) i.v. 10 min before reperfusion, or with anti-ANXA antiserum (0.2 ml of hyperimmune serum/animal), or the Cys-LT antagonist Montelukast (5 mg/kg,) (23) s.c. 30 min before reperfusion.…”

Section: Treatment Protocolsmentioning

confidence: 99%

“…To inhibit lipoxin action, we used two different strategies, an inhibitor of 5-lipoxygenase (ZM230487), a central enzyme in lipoxin biosynthesis, and BOC-1, an antagonist of the ALX receptor (27). Postischemic treatment of germfree mice with ZM230487 (5.0 mg/kg) or BOC-1 (2.0 mg/kg) was accompanied by a significant increase in reperfusion-induced tissue injury, as assessed by intestinal (Fig.…”

Section: Inhibition Of Lxa 4 Partially Reverses the Inflammatory Hypomentioning

confidence: 99%

“…3 and 4). There is evidence showing that both LXA 4 and ANXA-1 may share the same receptor, ALX, and that effects mediated by this receptor can be inhibited by BOC-1 (27,30). To examine whether a combined action of LXA 4 and ANXA-1 would be sufficient to fully activate the ALX receptor and mediate the inflammatory responsiveness of germfree mice, we administered ZM230487 and anti-ANXA-1 Ab concomitantly to germfree mice submitted to intestinal ischemia and reperfusion.…”

Section: Simultaneous Inhibition Of Lxa 4 and Anxa-1 Prevents Il-10 Pmentioning

confidence: 99%

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The Required Role of Endogenously Produced Lipoxin A4 and Annexin-1 for the Production of IL-10 and Inflammatory Hyporesponsiveness in Mice

Souza¹,

Fagundes²,

Amaral³

et al. 2007

The Journal of Immunology

122

114

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The appropriate development of an inflammatory response is central for the ability of a host to deal with any infectious insult. However, excessive, misplaced, or uncontrolled inflammation may lead to acute or chronic diseases. The microbiota plays an important role in the control of inflammatory responsiveness. In this study, we investigated the role of lipoxin A4 and annexin-1 for the IL-10-dependent inflammatory hyporesponsiveness observed in germfree mice. Administration of a 15-epi-lipoxin A4 analog or an annexin-1-derived peptide to conventional mice prevented tissue injury, TNF-α production, and lethality after intestinal ischemia/reperfusion. This was associated with enhanced IL-10 production. Lipoxin A4 and annexin-1 failed to prevent reperfusion injury in IL-10-deficient mice. In germfree mice, there was enhanced expression of both lipoxin A4 and annexin-1. Blockade of lipoxin A4 synthesis with a 5-lipoxygenase inhibitor or Abs against annexin-1 partially prevented IL-10 production and this was accompanied by partial reversion of inflammatory hyporesponsiveness in germfree mice. Administration of BOC-1, an antagonist of ALX receptors (at which both lipoxin A4 and annexin-1 act), or simultaneous administration of 5-lipoxygenase inhibitor and anti-annexin-1 Abs, was associated with tissue injury, TNF-α production, and lethality similar to that found in conventional mice. Thus, our data demonstrate that inflammatory responsiveness is tightly controlled by the presence of the microbiota and that the innate capacity of germfree mice to produce IL-10 is secondary to their endogenous greater ability to produce lipoxin A4 and annexin-1.

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Involvement of the Receptor for Formylated Peptides in the in Vivo Anti-Migratory Actions of Annexin 1 and its Mimetics

Cited by 112 publications

References 34 publications

Annexin 1 Released by Necrotic Human Glioblastoma Cells Stimulates Tumor Cell Growth through the Formyl Peptide Receptor 1

Annexin 1 Released by Necrotic Human Glioblastoma Cells Stimulates Tumor Cell Growth through the Formyl Peptide Receptor 1

Anti-inflammatory functions of glucocorticoid-induced genes

The Required Role of Endogenously Produced Lipoxin A4 and Annexin-1 for the Production of IL-10 and Inflammatory Hyporesponsiveness in Mice

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