Annexin 1-Derived Peptide Ac2-26 Inhibits Eosinophil Recruitment in vivo via Decreasing Prostaglandin D&lt;sub&gt;2&lt;/sub&gt;

Wang, Lianming; Li, Wenhui; Xu, Yan; Wei, Qiang; Zhao, Hongbo; Jiang, Xiaofeng

doi:10.1159/000320228

Cited by 20 publications

(11 citation statements)

References 35 publications

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“…Because antibody binding to surface-associated proteins can inhibit fusion by steric hindrance even if the antigens are not involved in fusion, we tested an alternative approach to block Anx A1 and A5 activities by the peptides comprising N-terminal regions of these Anxs. A1-peptide has been demonstrated to inhibit several Anx A1dependent processes (McNeil et al, 2006;Wang et al, 2011). Here we show that this peptide and an A5-peptide inhibited lipid mixing and syncytium formation by primary myoblasts (Fig.…”

Section: Experimental System and Fusion Pathwaysupporting

confidence: 59%

Extracellular annexins and dynamin are important for sequential steps in myoblast fusion

Leikina¹,

Melikov²,

Sanyal³

et al. 2013

J Gen Physiol

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Section: Experimental System and Fusion Pathwaysupporting

confidence: 59%

Extracellular annexins and dynamin are important for sequential steps in myoblast fusion

Leikina¹,

Melikov²,

Sanyal³

et al. 2013

J Gen Physiol

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“…This peptide inhibited mast cell degranulation and neutrophil and eosinophil recruitment, and it prevented the release of histamines and eotaxins which are precursor mediators. This condition suggests that derivatives of ANXA1 can be used in the presence of allergic inflammation [28,29]. …”

Section: Discussionmentioning

confidence: 99%

Decreased Levels of Lipoxin A4 and Annexin A1 in Wheezy Infants

Gungor

Tahan

Gökahmetoğlu

et al. 2014

Int Arch Allergy Immunol

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Objective: Wheezing is a common and challenging health issue in infancy and early childhood. Asthma diagnosis is frequent in patients with a history of recurrent wheezing. A relationship has been reported between asthma and anti-inflammatory mediators such as lipoxin A4 and annexin A1. However, this remains uncertain in wheezy infants. The aim of the present study was to determine lipoxin A4 and annexin A1 levels in wheezy infants. Materials and Methods: Eighty-seven patients aged 6-36 months were included in this study. Demographic characteristics, clinical features, laboratory data, clinical diagnoses, and treatments, if present, were recorded. Patients were divided into 2 groups: patients with wheezing (n = 59) and healthy controls (n = 28). Blood samples were taken and lipoxin A4 and annexin A1 levels were evaluated by ELISA. Results: Lipoxin A4 and annexin A1 levels were significantly lower in the wheezing group than in the control group (p < 0.05). A significant correlation was found between the serum total immunoglobulin E (IgE) level and the percentage and absolute number of eosinophils (p < 0.05). No significant correlation was found in terms of lipoxin A4 and annexin A1 levels, the serum total IgE level, and the percentage and absolute number of eosinophils among groups (p > 0.05). Conclusion: This is the first study to assess lipoxin A4 and annexin A1 levels in wheezy infants. The levels of lipoxin A4 and annexin A1 were found to be low in wheezy infants. We hope that these results will lead to novel therapeutic options for asthma in cases where an optimal treatment modality is lacking.

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“…Ac2-26 is effective in a range of anti-inflammatory assays including models of ocular inflammation and asthma at doses of 1 mg/kg (30,31), but the structure has not been reported. We show here that the N-terminal region, including the MC-12 sequence (residues 9 -11), is well defined in contrast to the C-terminal region of the peptide (Fig.…”

Section: Novel Anti-inflammatory Peptidementioning

confidence: 99%

An engineered cyclic peptide alleviates symptoms of inflammation in a murine model of inflammatory bowel disease

Caceres

Bansal

Navarro

et al. 2017

Journal of Biological Chemistry

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Edited by Wolfgang PetiInflammatory bowel diseases (IBDs) are a set of complex and debilitating diseases for which there is no satisfactory treatment. Recent studies have shown that small peptides show promise for reducing inflammation in models of IBD. However, these small peptides are likely to be unstable and rapidly cleared from the circulation, and therefore, if not modified for better stability, represent non-viable drug leads. We hypothesized that improving the stability of these peptides by grafting them into a stable cyclic peptide scaffold may enhance their therapeutic potential. Using this approach, we have designed a novel cyclic peptide that comprises a small bioactive peptide from the annexin A1 protein grafted into a sunflower trypsin inhibitor cyclic scaffold. We used native chemical ligation to synthesize the grafted cyclic peptide. This engineered cyclic peptide maintained the overall fold of the naturally occurring cyclic peptide, was more effective at reducing inflammation in a mouse model of acute colitis than the bioactive peptide alone, and showed enhanced stability in human serum. Our findings suggest that the use of cyclic peptides as structural backbones offers a promising approach for the treatment of IBD and potentially other chronic inflammatory conditions. Inflammatory bowel diseases (IBDs)3 are a set of chronic inflammatory disorders of the gastrointestinal tract; the two major forms are ulcerative colitis and Crohn's disease (1). Although there are several medications on the market for IBD, they generally only provide temporary relief, and 70% of IBD patients require surgical intervention (2). Because the current treatments are not satisfactory, new drug leads are being sought from a range of sources, including small molecules from plants and bioactive regions of larger proteins (3-6).Intriguingly, several small peptides, some comprising only three residues, have been shown to be effective in the treatment of experimental colitis in mice (7-11). One example is a tripeptide (MC-12) derived from annexin A1, a calcium-dependent phospholipid-binding, anti-inflammatory protein (12). Annexin A1 mediates expression of cytokines such as TNF-␣, IL-6, and IL-10. It is required for the inhibition of NF-B activity by anti-inflammatory drugs (13) and has recently been shown to be a potential biomarker of therapeutic efficacy for IBD (14). The N-terminal region of annexin A1 comprising residues 2-26 (Ac2-26) has been well studied (15, 16) and appears to have the same biological effects as the full-length protein (17). Analysis of a series of peptides based on the N-terminal sequence of annexin A1 showed that MC-12 (Ac-Gln-Ala-Trp) was the most potent inhibitor of NF-B activity in SW480 cells (13).Small peptides such as MC-12 are likely to be unstable and not viable drug leads, supported by the finding that high doses (25 mg/kg) of MC-12 were required to elicit an in vivo response in mouse colitis models, and it was more effective when injected compared with oral administration (18). Improving t...

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Annexin 1-Derived Peptide Ac2-26 Inhibits Eosinophil Recruitment in vivo via Decreasing Prostaglandin D<sub>2</sub>

Cited by 20 publications

References 35 publications

Extracellular annexins and dynamin are important for sequential steps in myoblast fusion

Extracellular annexins and dynamin are important for sequential steps in myoblast fusion

Decreased Levels of Lipoxin A4 and Annexin A1 in Wheezy Infants

An engineered cyclic peptide alleviates symptoms of inflammation in a murine model of inflammatory bowel disease

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