Neutrophils and neutrophil extracellular traps enhance venous thrombosis in mice bearing human pancreatic tumors

Hisada, Yohei; Grover, Steven P.; Maqsood, Anaum; Houston, Reaves; Ay, Cihan; Noubouossié, Denis; Cooley, Brian C.; Wallén, Håkan; Key, Nigel S.; Thålin, Charlotte; Farkas, A.; Farkas, Veronika J.; Tenekedjiev, Kiril; Kolev, Krasimir; Mackman, Nigel

doi:10.3324/haematol.2019.217083

Cited by 119 publications

(115 citation statements)

References 47 publications

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“…Conversely, tumor cells may activate neutrophils, thereby stimulating NETosis as shown in vitro and in mouse tumor models [248,253]. Another mechanism by which NETs favor CTC survival and colonization is through their ability to activate coagulation and thrombosis [254][255][256][257][258]. NETs have indeed been shown to activate platelets.…”

Section: Interaction With Neutrophilsmentioning

confidence: 99%

EMT-Associated Heterogeneity in Circulating Tumor Cells: Sticky Friends on the Road to Metastasis

Genna

Vanwynsberghe

Villard

et al. 2020

Cancers

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Epithelial–mesenchymal transitions (EMTs) generate hybrid phenotypes with an enhanced ability to adapt to diverse microenvironments encountered during the metastatic spread. Accordingly, EMTs play a crucial role in the biology of circulating tumor cells (CTCs) and contribute to their heterogeneity. Here, we review major EMT-driven properties that may help hybrid Epithelial/Mesenchymal CTCs to survive in the bloodstream and accomplish early phases of metastatic colonization. We then discuss how interrogating EMT in CTCs as a companion biomarker could help refine cancer patient management, further supporting the relevance of CTCs in personalized medicine.

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Section: Interaction With Neutrophilsmentioning

confidence: 99%

EMT-Associated Heterogeneity in Circulating Tumor Cells: Sticky Friends on the Road to Metastasis

Genna

Vanwynsberghe

Villard

et al. 2020

Cancers

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“…The IVC stasis model was conducted as previously described. 22,23 Mice were anesthetized by intraperitoneal injection of ketamine (100 mg/kg) and xylazine (10 mg/kg). A midline laparotomy was made and the bowel externalized and wrapped in wetted gauze.…”

Section: Ivc Stasis Modelmentioning

confidence: 99%

Model‐dependent contributions of FXII and FXI to venous thrombosis in mice

Grover

Olson

Cooley

et al. 2020

Journal of Thrombosis and Haemostasis

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“…NETosis has been found in response to various stimuli such as LPS, damage-associated molecular patterns (DAMPs), and PMA [6,8]. Recent studies have implicated that neutrophils play an essential role in the control of sterile inflammatory diseases, which are also characterized by a sustained influx of neutrophils and persistent NET release, and contribute to various injury processes [9,10]. For instance, in chronic obstructive pulmonary disease and cystic fibrosis, neutrophils and NETs contribute to chronic inflammatory and lung tissue damage [11,12].…”

Section: Introductionmentioning

confidence: 99%

Neutrophil Chemotaxis and NETosis in Murine Chronic Liver Injury via Cannabinoid Receptor 1/Gαi/o/ROS/p38 MAPK Signaling Pathway

Zhou

Yang

Fan

et al. 2020

Cells

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Neutrophils play an essential role in the control of inflammatory diseases. However, whether cannabinoid receptors (CBs) play a role in neutrophil chemotaxis and NETosis in sterile liver inflammation remains unknown. The expression of marker genes on neutrophils was characterized by FACS, immunofluorescence, qRT-PCR, and Western blot. The amount of neutrophils was significantly elevated from 7 days and reached the peak at 2 weeks in carbon tetrachloride (CCl4)-treated mouse liver. The mRNA expression of neutrophil marker Ly6G had positive correlation with CB1 and CB2 expression in injured liver. In vitro CBs were abundantly expressed in isolated neutrophils and CB1 agonist ACEA promoted the chemotaxis and cytoskeletal remodeling, which can be suppressed by CB1 antagonist AM281. Moreover, ACEA induced NETosis, myeloperoxidase release from lysosome and ROS burst, indicating neutrophil activation, via Gαi/o. Conversely, CB2 agonist JWH133 had no effect on neutrophil function. ROS and p38 MAPK signaling pathways were involved in CB1-mediated neutrophil function, and ROS was upstream of p38 MAPK. CB1 blockade in vivo significantly attenuated neutrophil infiltration and liver inflammation in CCl4-treated mice. Taken together, CB1 mediates neutrophil chemotaxis and NETosis via Gαi/o/ROS/p38 MAPK signaling pathway in liver inflammation, which represents an effective therapeutic strategy for liver diseases.

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Neutrophils and neutrophil extracellular traps enhance venous thrombosis in mice bearing human pancreatic tumors

Cited by 119 publications

References 47 publications

EMT-Associated Heterogeneity in Circulating Tumor Cells: Sticky Friends on the Road to Metastasis

EMT-Associated Heterogeneity in Circulating Tumor Cells: Sticky Friends on the Road to Metastasis

Model‐dependent contributions of FXII and FXI to venous thrombosis in mice

Neutrophil Chemotaxis and NETosis in Murine Chronic Liver Injury via Cannabinoid Receptor 1/Gαi/o/ROS/p38 MAPK Signaling Pathway

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