Annexin A1: shifting the balance towards resolution and repair

Leoni, Giovanna; Nusrat, Asma

doi:10.1515/hsz-2016-0180

Cited by 59 publications

(57 citation statements)

References 89 publications

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“…In this system, Annexin A6 is recruited to the membrane, leading to the formation of a “repair cap” that allows for membrane reorganization and eventual resealing, thereby healing the injury (Swaggart et al, 2014). This property of membrane repair also extends to another Annexin, Annexin A1, in epithelia and immune cells, where it orchestrates repair mechanisms during mucosal homeostasis (Leoni and Nusrat, 2016). Similarly, in mammalian myofibers upon plasma membrane injury, several Annexins (A1, A2, A5, A6) form a tight repair cap complex that is actin-dependent (Demonbreun et al, 2016).…”

Section: Discussionmentioning

confidence: 93%

Annexin A6 controls neuronal membrane dynamics throughout chick cranial sensory gangliogenesis

Shah

Schiffmacher

Taneyhill

2017

Developmental Biology

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Cranial sensory ganglia are components of the peripheral nervous system that possess a significant somatosensory role and include neurons within the trigeminal and epibranchial nerve bundles. Although it is well established that these ganglia arise from interactions between neural crest and neurogenic placode cells, the molecular basis of ganglia assembly is still poorly understood. Members of the Annexin protein superfamily play key roles in sensory nervous system development throughout metazoans. Annexin A6 is expressed in chick trigeminal and epibranchial placode cell-derived neuroblasts and neurons, but its function in cranial ganglia formation has not been elucidated. To this end, we interrogated the role of Annexin A6 using gene perturbation studies in the chick embryo. Our data reveal that placode cell-derived neuroblasts with reduced Annexin A6 levels ingress and migrate normally to the ganglionic anlage, where neural crest cell corridors correctly form around them. Strikingly, while Annexin A6-depleted placode cell-derived neurons still express mature neuronal markers, they fail to form two long processes, which are considered morphological features of mature neurons, and no longer innervate their designated targets due to the absence of this bipolar morphology. Moreover, overexpression of Annexin A6 causes some placode cell-derived neurons to form extra protrusions alongside these bipolar processes. These data demonstrate that the molecular program associated with neuronal maturation is distinct from that orchestrating changes in neuronal morphology, and, importantly, reveal Annexin A6 to be a key membrane scaffolding protein during sensory neuron membrane biogenesis. Collectively, our results provide novel insight into mechanisms underscoring morphological changes within placode cell-derived neurons that are essential for cranial gangliogenesis.

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Section: Discussionmentioning

confidence: 93%

Annexin A6 controls neuronal membrane dynamics throughout chick cranial sensory gangliogenesis

Shah

Schiffmacher

Taneyhill

2017

Developmental Biology

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“…EV represent a way of cellular communication and transfer of components which may be exploited for therapeutic purposes. In this regard, annexin A1 is secreted, at least in part, in EV by different cell types such as neutrophils [50] or human bone marrow mesenchymal stem cells [51] and it can be delivered into the recipient cell [50, 52]. Although further studies are needed to assess the possible contribution of other components of AD-MSC EV, our data suggest that annexin A1 may contribute to the anti-inflammatory and chondroprotective effects of these microparticles under inflammatory stress conditions.…”

Section: Discussionmentioning

confidence: 99%

Microvesicles from Human Adipose Tissue-Derived Mesenchymal Stem Cells as a New Protective Strategy in Osteoarthritic Chondrocytes

Tofiño-Vian

Guillén

Caz

et al. 2018

Cell Physiol Biochem

175

141

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Background/Aims: Chronic inflammation contributes to cartilage degeneration during the progression of osteoarthritis (OA). Adipose tissue-derived mesenchymal stem cells (AD-MSC) show great potential to treat inflammatory and degradative processes in OA and have demonstrated paracrine effects in chondrocytes. In the present work, we have isolated and characterized the extracellular vesicles from human AD-MSC to investigate their role in the chondroprotective actions of these cells. Methods: AD-MSC were isolated by collagenase treatment from adipose tissue from healthy individuals subjected to abdominal lipectomy surgery. Microvesicles and exosomes were obtained from conditioned medium by filtration and differential centrifugation. Chondrocytes from OA patients were used in primary culture and stimulated with 10 ng/ml interleukin(IL)-1β in the presence or absence of AD-MSC microvesicles, exosomes or conditioned medium. Protein expression was investigated by ELISA and immunofluorescence, transcription factor-DNA binding by ELISA, gene expression by real-time PCR, prostaglandin E₂ (PGE₂) by radioimmunoassay, and matrix metalloproteinase (MMP) activity and nitric oxide (NO) production by fluorometry. Results: In OA chondrocytes stimulated with IL-1β, microvesicles and exosomes reduced the production of inflammatory mediators tumor necrosis factor-α, IL-6, PGE₂ and NO. The downregulation of cyclooxygenase-2 and microsomal prostaglandin E synthase-1 would lead to the decreased PGE₂ production while the effect on NO could depend on the reduction of inducible nitric oxide synthase expression. Treatment of OA chondrocytes with extracellular vesicles also decreased the release of MMP activity and MMP-13 expression whereas the production of the anti-inflammatory cytokine IL-10 and the expression of collagen II were significantly enhanced. The reduction of inflammatory and catabolic mediators could be the consequence of a lower activation of nuclear factor-κB and activator protein-1. The upregulation of annexin A1 specially in MV may contribute to the anti-inflammatory and chondroprotective effects of AD-MSC. Conclusions: Our data support the interest of AD-MSC extracellular vesicles to develop new therapeutic approaches in joint conditions.

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“…18,20,23 Moreover, AnxA1 is also involved in maintaining tissue integrity during inflammation. 37,38 Though this mediator is undoubtedly an important regulator of the host response, its specific role in pneumococcal pneumonia has not been investigated. In this study, we uncover the nonredundant role of AnxA1 and its receptor FPR2 in controlling the inflammatory response and bacterial proliferation during S pneumoniae pulmonary infection.…”

Section: Discussionmentioning

confidence: 99%

The Annexin A1/FPR2 pathway controls the inflammatory response and bacterial dissemination in experimental pneumococcal pneumonia

et al. 2019

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Streptococcus pneumoniae is a major cause of community-acquired pneumonia leading to high mortality rates. Inflammation triggered by pneumococcal infection is necessary for bacterial clearance but must be spatially and temporally regulated to prevent further tissue damage and bacterial dissemination. Annexin A1 (AnxA1) mainly acts through Formyl Peptide Receptor 2 (FPR2) inducing the resolution of inflammation. Here, we have evaluated the role of AnxA1 and FPR2 during pneumococcal pneumonia in mice. For that, AnxA1, Fpr2/3 knockout (KO) mice and wild-type (WT) controls were infected intranasally with S pneumoniae. AnxA1 and Fpr2/3 KO mice were highly susceptible to infection, displaying uncontrolled inflammation, increased bacterial dissemination, and pulmonary dysfunction compared to WT animals. Mechanistically, the absence of AnxA1 resulted in the loss of lung barrier integrity and increased neutrophil activation upon S pneumoniae stimulation.Importantly, treatment of WT or AnxA1 KO-infected mice with Ac2-26 decreased inflammation, lung damage, and bacterial burden in the airways by increasing 2750 | MACHADO et Al.

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Annexin A1: shifting the balance towards resolution and repair

Cited by 59 publications

References 89 publications

Annexin A6 controls neuronal membrane dynamics throughout chick cranial sensory gangliogenesis

Annexin A6 controls neuronal membrane dynamics throughout chick cranial sensory gangliogenesis

Microvesicles from Human Adipose Tissue-Derived Mesenchymal Stem Cells as a New Protective Strategy in Osteoarthritic Chondrocytes

The Annexin A1/FPR2 pathway controls the inflammatory response and bacterial dissemination in experimental pneumococcal pneumonia

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