| dc.creator | Araya, Paulina | |
| dc.creator | Romero, Jacqueline | |
| dc.creator | Delgado-López, Fernando | |
| dc.creator | Gonzalez, Ileana | |
| dc.creator | Añazco-Oyarzún, Carolina | |
| dc.creator | Perez, Ramón | |
| dc.creator | Rojas, Armando | |
| dc.date | 2023-01-23T18:01:54Z | |
| dc.date | 2023-01-23T18:01:54Z | |
| dc.date | 2019 | |
| dc.date.accessioned | 2024-05-02T20:30:30Z | |
| dc.date.available | 2024-05-02T20:30:30Z | |
| dc.identifier | http://repositorio.ucm.cl/handle/ucm/4429 | |
| dc.identifier.uri | https://repositorioslatinoamericanos.uchile.cl/handle/2250/9274672 | |
| dc.description | 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. | |
| dc.language | en | |
| dc.rights | Atribución-NoComercial-SinDerivadas 3.0 Chile | |
| dc.rights | http://creativecommons.org/licenses/by-nc-nd/3.0/cl/ | |
| dc.source | Inflammation Research, 68(8), 639-642 | |
| dc.title | HMGB1 decreases CCR-2 expression and migration of M2 macrophages under hypoxia | |
| dc.type | Article | |
