In vitro and in vivo studies on CCR10 regulation by Annexin A1

Rodrigues-Lisoni, Flávia Cristina; Mehemet, Devinder K.; Peitl, Paulo; John, Christopher; Tajara, Eloíza H.; Buckingham, Julia C.; Solito, Egle

doi:10.1016/j.febslet.2006.01.072

Cited by 16 publications

(13 citation statements)

References 38 publications

(48 reference statements)

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“…Hyperglycaemia leads to activation (phosphorylation) of mitogen-activated protein kinases (MAPKs) p38, JNK and ERK1/2, hypertrophy and fibrosis in the heart [32][33][34][35][36][37][38] and kidney [39,40]. While little evidence is available to suggest strong tissue specific activation of proinflammatory pathways in STZ-induced diabetes, pharmacological inhibition or genetic deletion of any of these three MAPKs reduces microvascular complications (diabetic nephropathy, cardiomyopathy and retinopathy) caused by type 1 diabetes in rodents [41,42].…”

Section: Discussionmentioning

confidence: 99%

“…Previously, both full-length AXNA1 and the Ac2-26 peptide (the N-terminal functional fragment of ANXA1) have been used in vivo and both elicit biological function [17][18][19]). In this study, we chose to use fulllength hrANXA1, as the dose of full-length ANXA1 needed to induce biological function is up to 20 times less than that of the Ac2-26 peptide [36] and 14 times less than that needed to induce changes in gene expression in terms of molarity [37].…”

Section: Discussionmentioning

confidence: 99%

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Annexin A1 attenuates microvascular complications through restoration of Akt signalling in a murine model of type 1 diabetes

et al. 2017

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Aims/hypothesis Microvascular complications in the heart and kidney are strongly associated with an overall rise in inflammation. Annexin A1 (ANXA1) is an endogenous anti-inflammatory molecule that limits and resolves inflammation. In this study, we have used a bedside to bench approach to investigate: (1) ANXA1 levels in individuals with type 1 diabetes; (2) the role of endogenous ANXA1 in nephropathy and cardiomyopathy in experimental type 1 diabetes; and (3) whether treatment with human recombinant ANXA1 attenuates nephropathy and cardiomyopathy in a murine model of type 1 diabetes. Methods ANXA1 was measured in plasma from individuals with type 1 diabetes with or without nephropathy and healthy donors. Experimental type 1 diabetes was induced in mice by injection of streptozotocin (STZ; 45 mg/kg i.v. per day for 5 consecutive days) in C57BL/6 or Anxa1 −/− mice. Diabetic mice were treated with human recombinant (hr)ANXA1(1 μg, 100 μl, 50 mmol/l HEPES; 140 mmol/l NaCl; pH 7.4, i.p.) or vehicle (100 μl, 50 mmol/l HEPES; 140 mmol/l NaCl; pH 7.4, i.p.).Results Plasma levels of ANXA1 were elevated in individuals with type 1 diabetes with/without nephropathy compared with healthy individuals (66.0 ± 4.2/64.0 ± 4 ng/ml vs 35.9 ± 2.3 ng/ml; p < 0.05). Compared with diabetic wild-type (WT) mice, diabetic Anxa1 −/− mice exhibited a worse diabetic phenotype and developed more severe cardiac (ejection fraction; 76.1 ± 1.6% vs 49.9 ± 0.9%) and renal dysfunction (proteinuria; 89.3 ± 5.0 μg/ mg vs 113.3 ± 5.5 μg/mg). Mechanistically, compared with nondiabetic WT mice, the degree of the phosphorylation of mitogenactivated protein kinases (MAPKs) p38, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) was significantly higher in non-diabetic Anxa1 −/− mice in both the heart and kidney, and was further enhanced after STZ-induced type 1 diabetes. Prophylactic treatment with hrANXA1 (weeks 1-13) attenuated both cardiac (ejection fraction; 54.0 ± 1.6% vs 72.4 ± 1.0%) and renal (proteinuria; 89.3 ± 5.0 μg/mg vs 53.1 ± 3.4 μg/mg) dysfunction associated with STZ-induced diabetes, while therapeutic administration of hrANXA1 (weeks 8-13), after significant cardiac and renal dysfunction had already developed, halted the further functional decline in cardiac and renal function seen in diabetic mice administered vehicle. In addition, administration of hrANXA1 attenuated the increase in phosphorylation of p38, JNK and ERK, and restored phosphorylation of Akt in diabetic mice. Conclusions/interpretationOverall, these results demonstrate that ANXA1 plasma levels are elevated in individuals with Christoph Thiemermann and Egle Solito contributed equally to this work.Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00125-017-4469-y) contains peer-reviewed but unedited supplementary material, which is available to authorised users.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Annexin A1 attenuates microvascular complications through restoration of Akt signalling in a murine model of type 1 diabetes

et al. 2017

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“…31 The yet unknown mechanism by which ANXA1 regulates proliferation might involve gene expression modulation since recent data support such a role for this protein. 32 It is also possible that and in broncho-alveolar epithelial cells. 36 In addition, ANXA1 expression is strongly induced in thyroid carcinoma cells during ''tumor necrosis factor-related apoptosis inducing ligand'' (TRAIL)-induced apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Annexin 1: Differential expression in tumor and mast cells in human larynx cancer

Silistino-Souza

Rodrigues-Lisoni

Cury

et al. 2007

Intl Journal of Cancer

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Annexin 1 protein (ANXA1) expression was evaluated in tumor and mast cells in human larynx cancer and control epithelium. The effect of the exogenous ANXA1 (peptide Ac 2-26) was also examined during the cellular growth of the Hep-2 human larynx epidermoid carcinoma cell line. This peptide inhibited the proliferation of the Hep-2 cells within 144 hr. In surgical tissue specimens from 20 patients with larynx cancer, ultrastructural immunocytochemistry analysis showed in vivo down-regulation of ANXA1 expression in the tumor and increased in mast cells and Hep-2 cells treated with peptide Ac2-26. Combined in vivo and in vitro analysis demonstrated that ANXA1 plays a regulatory role in laryngeal cancer cell growth. We believe that a better understanding of the regulatory mechanisms of ANXA1 in tumor and mast cells may lead to future biological targets for the therapeutic intervention of human larynx cancer. ' 2007 Wiley-Liss, Inc.

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“…TNF-alpha and NF-κB transcription factor should play a central role in this process, modulating transcription of genes encoding angiogenic and growth factors, inflammatory cytokines and anti-apoptotic proteins [16]. In fact, many inflammatory mediators may influence cell proliferation and tumor development, as demonstrated by our recent studies on annexin A1 [18-20]. …”

Section: Introductionmentioning

confidence: 99%

Genomics and proteomics approaches to the study of cancer-stroma interactions

et al. 2010

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BackgroundThe development and progression of cancer depend on its genetic characteristics as well as on the interactions with its microenvironment. Understanding these interactions may contribute to diagnostic and prognostic evaluations and to the development of new cancer therapies. Aiming to investigate potential mechanisms by which the tumor microenvironment might contribute to a cancer phenotype, we evaluated soluble paracrine factors produced by stromal and neoplastic cells which may influence proliferation and gene and protein expression.MethodsThe study was carried out on the epithelial cancer cell line (Hep-2) and fibroblasts isolated from a primary oral cancer. We combined a conditioned-medium technique with subtraction hybridization approach, quantitative PCR and proteomics, in order to evaluate gene and protein expression influenced by soluble paracrine factors produced by stromal and neoplastic cells.ResultsWe observed that conditioned medium from fibroblast cultures (FCM) inhibited proliferation and induced apoptosis in Hep-2 cells. In neoplastic cells, 41 genes and 5 proteins exhibited changes in expression levels in response to FCM and, in fibroblasts, 17 genes and 2 proteins showed down-regulation in response to conditioned medium from Hep-2 cells (HCM). Nine genes were selected and the expression results of 6 down-regulated genes (ARID4A, CALR, GNB2L1, RNF10, SQSTM1, USP9X) were validated by real time PCR.ConclusionsA significant and common denominator in the results was the potential induction of signaling changes associated with immune or inflammatory response in the absence of a specific protein.

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In vitro and in vivo studies on CCR10 regulation by Annexin A1

Cited by 16 publications

References 38 publications

Annexin A1 attenuates microvascular complications through restoration of Akt signalling in a murine model of type 1 diabetes

Annexin A1 attenuates microvascular complications through restoration of Akt signalling in a murine model of type 1 diabetes

Annexin 1: Differential expression in tumor and mast cells in human larynx cancer

Genomics and proteomics approaches to the study of cancer-stroma interactions

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