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See detailHypoxia-Induced Adaptations of miRNomes and Proteomes in Melanoma Cells and Their Secreted Extracellular Vesicles
Walbrecq, Geoffroy; Lecha, Odile; Gaigneaux, Anthoula UL et al

in Cancers (2020)

Reduced levels of intratumoural oxygen are associated with hypoxia-induced pro-oncogenic events such as invasion, metabolic reprogramming, epithelial–mesenchymal transition, metastasis and resistance to ... [more ▼]

Reduced levels of intratumoural oxygen are associated with hypoxia-induced pro-oncogenic events such as invasion, metabolic reprogramming, epithelial–mesenchymal transition, metastasis and resistance to therapy, all favouring cancer progression. Small extracellular vesicles (EV) shuttle various cargos (proteins, miRNAs, DNA and others). Tumour-derived EVs can be taken up by neighbouring or distant cells in the tumour microenvironment, thus facilitating intercellular communication. The quantity of extracellular vesicle secretion and their composition can vary with changing microenvironmental conditions and disease states. Here, we investigated in melanoma cells the influence of hypoxia on the content and number of secreted EVs. Whole miRNome and proteome profiling revealed distinct expression patterns in normoxic or hypoxic growth conditions. Apart from the well-known miR-210, we identified miR-1290 as a novel hypoxia-associated microRNA, which was highly abundant in hypoxic EVs. On the other hand, miR-23a-5p and -23b-5p were consistently downregulated in hypoxic conditions, while the protein levels of the miR-23a/b-5p-predicted targetIPO11were concomitantly upregulated. Furthermore, hypoxic melanoma EVs exhibit a signature consisting of six proteins (AKR7A2, DDX39B, EIF3C, FARSA, PRMT5, VARS), which were significantly associated with a poor prognosis for melanoma patients, indicating that proteins and/or miRNAs secreted by cancer cells may be exploited as biomarkers. [less ▲]

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See detailEarly life stress reduces neuropathic pain in adulthood -is alteration of spinal microglial reactivity critically involved?
Genty, Julien UL; Tetsi Nomigni, Milène UL; Anton, Fernand UL et al

Poster (2017, November 14)

Growing evidence underlines the association between early life adversity and persistent alterations of neural, endocrine and immune functions that may be accompanied by a host of disease patterns such as ... [more ▼]

Growing evidence underlines the association between early life adversity and persistent alterations of neural, endocrine and immune functions that may be accompanied by a host of disease patterns such as chronic pain in later life. Neuropathy is a debilitating condition presenting a substantial cooccurrence with stress related disorders. Despite the established overlapping of biochemical pathways involved in the etiology of these disorders, the intricacy of their mutual interdependence remains. In this context, immunocompetent cells are largely affected during chronic stress and are a key factor in the sensitization of nociceptive dorsal horn neurons. The goal of the present study was to investigate the impact of maternal separation (MS), a wellestablished model of early life stress in rodents, on chronic constriction injury (CCI)induced neuropathic pain and to reveal the relevance of spinal microglia activation and proinflammatory cytokine regulation. For this purpose 12 groups of rats were exposed to different combinations of stress condition, CCIinjury and pharmacological treatment. Noxious sensitivity was tested during baseline conditions as well as during subsequent neuropathic and pharmacological treatment conditions. Von Frey hair and the cold plate tests were used for the assessment of mechanical and cold hyperalgesia/allodynia. Amphotericin B, a substance known to activate monocytes and macrophages in the periphery and microglial cells in the CNS was administered to subgroups of animals. At the end of the protocol, rats were sacrificed to assess microglial activation using qPCR and immunohistochemistry. Our main finding was that maternal separation led to a reduction of CCIrelated pain hypersensitivity (thermal and mechanical hyperalgesia/allodynia). We concomitantly observed a downregulation of Iba 1, mRNA a marker of microglial cells, and of IL1β mRNA, a proinflammatory cytokine that may be released by microglia. According to preliminary results, Amphotericin B in turn seemed to enhance CCI related pain sensitivity, possibly via an activation of microglia. Our results show that MS may lead to a reduction of neuropathy relatedpain in adult age. Stress related dampening of spinal microglial reactivity may play a critical role in this context. [less ▲]

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