Lipoxin A4 Stimulates a Cytosolic Ca2+Increase in Human Bronchial Epithelium

Bonnans, Caroline; Mainprice, B.; Chanez, Pascal; Bousquet, Jean; Urbach, V.

doi:10.1074/jbc.m210294200

Cited by 61 publications

(70 citation statements)

References 39 publications

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“…Furthermore, it has been reported that LXA 4 triggers epithelial cell migration, proliferation, and tight junction formation in several types of epithelia including the airway epithelium (3,13,21). It has been reported that levels of LXA 4 are reduced in CF airways (19). These observations suggest that the reduced capacity for epithelial repair described in the CF epithelium may be exacerbated or caused by low levels of LXA 4 (1,19,45).…”

mentioning

confidence: 62%

“…It has been reported that levels of LXA 4 are reduced in CF airways (19). These observations suggest that the reduced capacity for epithelial repair described in the CF epithelium may be exacerbated or caused by low levels of LXA 4 (1,19,45).…”

mentioning

confidence: 78%

“…In addition, lipoxin A 4 (LXA 4 ) has been reported to have other functions such as regulation of airway epithelial ion transport and airway surface liquid layer dynamics in CF (4,15,46). Furthermore, it has been reported that LXA 4 triggers epithelial cell migration, proliferation, and tight junction formation in several types of epithelia including the airway epithelium (3,13,21).…”

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confidence: 99%

“…In corneal models, it has been shown that LXA 4 partially stimulates repair through ERK phosphorylation (3,13,21). Additionally, many studies indicate that ion channels are involved in two key processes of repair, migration and proliferation (23).…”

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confidence: 99%

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Lipoxin A₄-mediated K_ATP potassium channel activation results in cystic fibrosis airway epithelial repair

Buchanan

McNally

Harvey

et al. 2013

American Journal of Physiology-Lung Cellular and Molecular Phys

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Buchanan PJ, McNally P, Harvey BJ, Urbach V. Lipoxin A4-mediated K ATP potassium channel activation results in cystic fibrosis airway epithelial repair. Am J Physiol Lung Cell Mol Physiol 305: L193-L201, 2013. First published May 17, 2013 doi:10.1152/ajplung.00058.2013The main cause of morbidity and mortality in cystic fibrosis (CF) is progressive lung destruction as a result of persistent bacterial infection and inflammation, coupled with reduced capacity for epithelial repair. Levels of the anti-inflammatory mediator lipoxin A4 (LXA4) have been reported to be reduced in bronchoalveolar lavages of patients with CF. We investigated the ability of LXA4 to trigger epithelial repair through the initiation of proliferation and migration in non-CF (NuLi-1) and CF (CuFi-1) airway epithelia. Spontaneous repair and cell migration were significantly slower in CF epithelial cultures (CuFi-1) compared with controls (NuLi-1). LXA4 triggered an increase in migration, proliferation, and wound repair of non-CF and CF airway epithelia. These responses to LXA 4 were completely abolished by the ALX/FPR2 receptor antagonist, Boc2 and ALX/FPR2 siRNA. The KATP channel opener pinacidil mimicked the LXA4 effect on migration, proliferation, and epithelial repair, whereas the KATP channel inhibitor, glibenclamide, blocked the responses to LXA4. LXA4 did not affect potassium channel expression but significantly upregulated glibenclamide-sensitive (KATP) currents through the basolateral membrane of NuLi-1 and CuFi-1 cells. MAP kinase (ERK1/2) inhibitor, PD98059, also inhibited the LXA4-induced proliferation of NuLi-1 and CuFi-1 cells. Finally, both LXA4 and pinacidil stimulated ERK-MAP kinase phosphorylation, whereas the effect of LXA4 on ERK phosphorylation was inhibited by glibenclamide. Taken together, our results provided evidence for a role of LXA4 in triggering epithelial repair through stimulation of the ALX/FPR2 receptor, K ATP potassium channel activation, and ERK phosphorylation. This work suggests exogenous delivery of LXA4, restoring levels in patients with CF, perhaps as a potential therapeutic strategy.

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confidence: 62%

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confidence: 78%

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confidence: 99%

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Lipoxin A₄-mediated K_ATP potassium channel activation results in cystic fibrosis airway epithelial repair

Buchanan

McNally

Harvey

et al. 2013

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Previous reports suggested the role of FPRL1 in the regulation of various cellular responses in several cell types: Ca 2ϩ -dependent Cl Ϫ secretion by human airway epithelial cells (2); the involvement in host defense in the brain by astrocytoma cell lines (3); the contribution to innate and adaptive immunities by recruiting neutrophils, monocytes, and T cells to sites of microbial invasion (4); and the induction of hyperadhesiveness in HUVECs to increase in the binding of neutrophils (5).…”

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confidence: 99%

Identification of Peptides That Antagonize Formyl Peptide Receptor-Like 1-Mediated Signaling

Bae

Lee

et al. 2004

The Journal of Immunology

150

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Formyl peptide receptor-like 1 (FPRL1) is an important classical chemoattractant receptor that is expressed in phagocytic cells in the peripheral blood and brain. Recently, various novel agonists have been identified from several origins, such as host-derived molecules. Activation of FPRL1 is closely related to inflammatory responses in the host defense mechanism and neurodegenerative disorders. In the present study we identified several novel peptides by screening hexapeptide libraries that inhibit the binding of one of FPRL1’s agonists (Trp-Lys-Tyr-Met-Val-d-Met-CONH2 (WKYMVm)) to its specific receptor, FPRL1, in RBL-2H3 cells. Among the novel peptides, Trp-Arg-Trp-Trp-Trp-Trp-CONH2 (WRWWWW (WRW4)) showed the most potent activity in terms of inhibiting WKYMVm binding to FPRL1. We also found that WRW4 inhibited the activation of FPRL1 by WKYMVm, resulting in the complete inhibition of the intracellular calcium increase, extracellular signal-regulated kinase activation, and chemotactic migration of cells toward WKYMVm. For the receptor specificity of WRW4 to the FPR family, we observed that WRW4 specifically inhibit the increase in intracellular calcium by the FPRL1 agonists MMK-1, amyloid β42 (Aβ42) peptide, and F peptide, but not by the FPR agonist, fMLF. To investigate the effect of WRW4 on endogenous FPRL1 ligand-induced cellular responses, we examined its effect on Aβ42 peptide in human neutrophils. Aβ42 peptide-induced superoxide generation and chemotactic migration of neutrophils were inhibited by WRW4, which also completely inhibited the internalization of Aβ42 peptide in human macrophages. WRW4 is the first specific FPRL1 antagonist and is expected to be useful in the study of FPRL1 signaling and in the development of drugs against FPRL1-related diseases.

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Beneficial Effects of Fish Oil on Human Brain

Farooqui¹

2009

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Lipoxin A4 Stimulates a Cytosolic Ca2+Increase in Human Bronchial Epithelium

Cited by 61 publications

References 39 publications

Lipoxin A₄-mediated K_ATP potassium channel activation results in cystic fibrosis airway epithelial repair

Lipoxin A₄-mediated K_ATP potassium channel activation results in cystic fibrosis airway epithelial repair

Identification of Peptides That Antagonize Formyl Peptide Receptor-Like 1-Mediated Signaling

Beneficial Effects of Fish Oil on Human Brain

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Lipoxin A4 Stimulates a Cytosolic Ca2+Increase in Human Bronchial Epithelium

Cited by 61 publications

References 39 publications

Lipoxin A4-mediated KATP potassium channel activation results in cystic fibrosis airway epithelial repair

Lipoxin A4-mediated KATP potassium channel activation results in cystic fibrosis airway epithelial repair

Identification of Peptides That Antagonize Formyl Peptide Receptor-Like 1-Mediated Signaling

Beneficial Effects of Fish Oil on Human Brain

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Product

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Lipoxin A₄-mediated K_ATP potassium channel activation results in cystic fibrosis airway epithelial repair

Lipoxin A₄-mediated K_ATP potassium channel activation results in cystic fibrosis airway epithelial repair