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HMGB1 decreases CCR-2 expression and migration of M2 macrophages under hypoxia
dc.contributor.author | Araya, Paulina | |
dc.contributor.author | Romero, Jacqueline | |
dc.contributor.author | Delgado-López, Fernando | |
dc.contributor.author | Gonzalez, Ileana | |
dc.contributor.author | Añazco-Oyarzún, Carolina | |
dc.contributor.author | Perez, Ramón | |
dc.contributor.author | Rojas, Armando | |
dc.date.accessioned | 2023-01-23T18:01:54Z | |
dc.date.available | 2023-01-23T18:01:54Z | |
dc.date.issued | 2019 | |
dc.identifier.uri | http://repositorio.ucm.cl/handle/ucm/4429 | |
dc.description.abstract | Objective: The hypoxic milieu at tumor microenvironment is able to drive the behavior of infiltrating tumor cells. Considering that hypoxia-mediated HMGB1 release is known to promote tumor growth, as well to enhance the pro-tumoral profile of M2 macrophages by a RAGE-dependent mechanism, it is tempting to evaluate the potential contribution of HMGB1 under hypoxia to restrain M2 macrophages mobility. Methods: CCR-2 expression was evaluated in M2 polarized macrophages by western blotting and immunocytochemistry. The secreted levels of CCL-2 and the migration capability were evaluated using an ELISA and a chemotaxis assay, respectively. Results: HMGB1, under hypoxic conditions, markedly reduce both the production of CCL-2 and the expression of its receptor CCR-2; and reduced the migration capacity of M2 macrophages. Conclusions: These results provided new insights into the mechanisms that regulate M2 macrophages mobility at the tumor microenvironment. | es_CL |
dc.language.iso | en | es_CL |
dc.rights | Atribución-NoComercial-SinDerivadas 3.0 Chile | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/3.0/cl/ | * |
dc.source | Inflammation Research, 68(8), 639-642 | es_CL |
dc.title | HMGB1 decreases CCR-2 expression and migration of M2 macrophages under hypoxia | es_CL |
dc.type | Article | es_CL |
dc.ucm.facultad | Facultad de Medicina | es_CL |
dc.ucm.indexacion | Scopus | es_CL |
dc.ucm.indexacion | Isi | es_CL |
dc.ucm.uri | link.springer.com/article/10.1007/s00011-019-01249-5 | es_CL |
dc.ucm.doi | doi.org/10.1007/s00011-019-01249-5 | es_CL |
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