Angiogenic factor-driven inflammation promotes extravasation of human proangiogenic monocytes to tumours

Autor: Marine Poittevin, Patricia Ropraz, Yalin Emre, Paul F. Bradfield, Adama Sidibé, Marc Pocard, Stephane Jemelin, Beat A. Imhof
Jazyk: angličtina
Rok vydání: 2018
Předmět:
0301 basic medicine
Vascular Endothelial Growth Factor A
Chemokine
Angiogenesis
medicine.medical_treatment
General Physics and Astronomy
Mice
SCID

ddc:616.07
Monocyte
Monocytes
Neovascularization
Patrolling
Cell Movement
Mice
Inbred NOD

Sein
lcsh:Science
Migration
Colorectal
Cancer
Non-classical
Multidisciplinary
biology
Neovascularization
Pathologic

Extravasation
medicine.anatomical_structure
Cytokine
Matrix Metalloproteinase 9
medicine.symptom
Colorectal Neoplasms
Science
CD14
Breast Neoplasms
GATA3 Transcription Factor
Adenocarcinoma
General Biochemistry
Genetics and Molecular Biology

Article
03 medical and health sciences
Interferon-gamma
Cell Line
Tumor

medicine
Animals
Humans
inflammation [Breast]
CX3CL1
ddc:612
Inflammation
business.industry
Chemokine CX3CL1
Tumor Necrosis Factor-alpha
General Chemistry
Leukocyte
030104 developmental biology
Cancer research
biology.protein
lcsh:Q
business
Neoplasm Transplantation
Zdroj: Nature Communications, Vol 9, Iss 1, Pp 1-19 (2018)
Nature Communications, Vol. 9, No 1 (2018) P. 19
Nature Communications
ISSN: 2041-1723
DOI: 10.1038/s41467-017-02610-0
Popis: Recruitment of circulating monocytes is critical for tumour angiogenesis. However, how human monocyte subpopulations extravasate to tumours is unclear. Here we show mechanisms of extravasation of human CD14dimCD16+ patrolling and CD14+CD16+ intermediate proangiogenic monocytes (HPMo), using human tumour xenograft models and live imaging of transmigration. IFNγ promotes an increase of the chemokine CX3CL1 on vessel lumen, imposing continuous crawling to HPMo and making these monocytes insensitive to chemokines required for their extravasation. Expression of the angiogenic factor VEGF and the inflammatory cytokine TNF by tumour cells enables HPMo extravasation by inducing GATA3-mediated repression of CX3CL1 expression. Recruited HPMo boosts angiogenesis by secreting MMP9 leading to release of matrix-bound VEGF-A, which amplifies the entry of more HPMo into tumours. Uncovering the extravasation cascade of HPMo sets the stage for future tumour therapies.
Circulating myeloid cells can leave the vasculature to infiltrate tumours and are thought to contribute to tumour angiogenesis. Here the authors live image monocytes that migrate to xenograft tumours and map an extravasation cascade of human proangiogenic monocytes into the tumour.
Databáze: OpenAIRE