| Title |
HMGB1 enhances the protumoral activities of M2 macrophages by a RAGE-dependent mechanism
|
|---|---|
| Published in |
Tumor Biology, October 2015
|
| DOI | 10.1007/s13277-015-3940-y |
| Pubmed ID | |
| Authors |
Armando Rojas, Fernando Delgado-López, Ramón Perez-Castro, Ileana Gonzalez, Jacqueline Romero, Israel Rojas, Paulina Araya, Carolina Añazco, Erik Morales, Jorge Llanos |
| Abstract |
The monocyte-macrophage lineage shows a high degree of diversity and plasticity. Once they infiltrate tissues, they may acquire two main functional phenotypes, being known as the classically activated type 1 macrophages (M1) and the alternative activated type 2 macrophages (M2). The M1 phenotype can be induced by bacterial products and interferon-γ and exerts a cytotoxic effect on cancer cells. Conversely, the alternatively activated M2 phenotype is induced by Il-4/IL13 and promotes tumor cell growth and vascularization. Although receptor for advanced glycation end-products (RAGE) engagement in M1 macrophages has been reported by several groups to promote inflammation, nothing is known about the functionality of RAGE in M2 macrophages. In the current study, we demonstrate that RAGE is equally expressed in both macrophage phenotypes and that RAGE activation by high-mobility group protein box1 (HMGB1) promotes protumoral activities of M2 macrophages. MKN45 cells co-cultured with M2 macrophages treated with HMGB1 at different times displayed higher invasive abilities. Additionally, conditioned medium from HMGB1-treated M2 macrophages promotes angiogenesis in vitro. RAGE-targeting knockdown abrogates these activities. Overall, the present findings suggest that HMGB1 may contribute, by a RAGE-dependent mechanism, to the protumoral activities of the M2 phenotype. |
X Demographics
The data shown below were collected from the profile of 1 X user who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Japan | 1 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Science communicators (journalists, bloggers, editors) | 1 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 40 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 40 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Ph. D. Student | 8 | 20% |
| Researcher | 7 | 18% |
| Student > Doctoral Student | 7 | 18% |
| Professor | 3 | 8% |
| Student > Master | 3 | 8% |
| Other | 7 | 18% |
| Unknown | 5 | 13% |
| Readers by discipline | Count | As % |
|---|---|---|
| Biochemistry, Genetics and Molecular Biology | 10 | 25% |
| Medicine and Dentistry | 6 | 15% |
| Agricultural and Biological Sciences | 5 | 13% |
| Engineering | 3 | 8% |
| Pharmacology, Toxicology and Pharmaceutical Science | 3 | 8% |
| Other | 4 | 10% |
| Unknown | 9 | 23% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 03 November 2015.
All research outputs
#18,428,159
of 22,829,683 outputs
Outputs from Tumor Biology
#1,369
of 2,622 outputs
Outputs of similar age
#199,992
of 277,991 outputs
Outputs of similar age from Tumor Biology
#109
of 255 outputs
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