scholarly journals Cellular Origins of the Lymphatic Endothelium: Implications for Cancer Lymphangiogenesis

2020 ◽  
Vol 11 ◽  
Author(s):  
Laura Gutierrez-Miranda ◽  
Karina Yaniv
2009 ◽  
Vol 183 (3) ◽  
pp. 1767-1779 ◽  
Author(s):  
Simona Podgrabinska ◽  
Okebugwu Kamalu ◽  
Lloyd Mayer ◽  
Motomu Shimaoka ◽  
Hans Snoeck ◽  
...  

Author(s):  
Silvano Sozzani ◽  
Annunciata Vecchi ◽  
Paola Allavena ◽  
Alberto Mantovani

2019 ◽  
Vol 10 (12) ◽  
Author(s):  
Audrey Zamora ◽  
Melinda Alves ◽  
Charlotte Chollet ◽  
Nicole Therville ◽  
Tiffany Fougeray ◽  
...  

AbstractCytotoxic therapy for breast cancer inhibits the growth of primary tumors, but promotes metastasis to the sentinel lymph nodes through the lymphatic system. However, the effect of first-line chemotherapy on the lymphatic endothelium has been poorly investigated. In this study, we determined that paclitaxel, the anti-cancer drug approved for the treatment of metastatic or locally advanced breast cancer, induces lymphatic endothelial cell (LEC) autophagy to increase metastases. While paclitaxel treatment was largely efficacious in inhibiting LEC adhesion, it had no effect on cell survival. Paclitaxel inhibited LEC migration and branch point formation by inducing an autophagy mechanism independent of Akt phosphorylation. In vivo, paclitaxel mediated a higher permeability of lymphatic endothelium to tumor cells and this effect was reversed by chloroquine, an autophagy-lysosome inhibitor. Despite a strong effect on reducing tumor size, paclitaxel significantly increased metastasis to the sentinel lymph nodes. This effect was restricted to a lymphatic dissemination, as chemotherapy did not affect the blood endothelium. Taken together, our findings suggest that the lymphatic system resists to chemotherapy through an autophagy mechanism to promote malignant progression and metastatic lesions. This study paves the way for new combinative therapies aimed at reducing the number of metastases.


2018 ◽  
Vol 2 (5) ◽  
pp. 701-712 ◽  
Author(s):  
Christina M. Warboys

Mechanical forces play an important role in regulating tissue development and homeostasis in multiple cell types including bone, joint, epithelial and vascular cells, and are also implicated in the development of diseases, e.g. osteoporosis, cardiovascular disease and osteoarthritis. Defining the mechanisms by which cells sense and respond to mechanical forces therefore has important implications for our understanding of tissue function in health and disease and may lead to the identification of targets for therapeutic intervention. Mechanoactivation of the Wnt signalling pathway was first identified in osteoblasts with a key role for β-catenin demonstrated in loading-induced osteogenesis. Since then, mechanoregulation of the Wnt pathway has also been observed in stem cells, epithelium, chondrocytes and vascular and lymphatic endothelium. Wnt can signal through both canonical and non-canonical pathways, and evidence suggests that both can mediate responses to mechanical strain, stretch and shear stress. This review will discuss our current understanding of the activation of the Wnt pathway in response to mechanical forces.


2019 ◽  
Vol 5 (6) ◽  
pp. eaaw5075 ◽  
Author(s):  
Guangchang Pei ◽  
Ying Yao ◽  
Qian Yang ◽  
Meng Wang ◽  
Yuxi Wang ◽  
...  

Lymphangiogenesis is associated with chronic kidney disease (CKD) and occurs following kidney transplant. Here, we demonstrate that expanding lymphatic vessels (LVs) in kidneys and corresponding renal draining lymph nodes (RDLNs) play critical roles in promoting intrarenal inflammation and fibrosis following renal injury. Our studies show that lymphangiogenesis in the kidney and RDLN is driven by proliferation of preexisting lymphatic endothelium expressing the essential C-C chemokine ligand 21 (CCL21). New injury-induced LVs also express CCL21, stimulating recruitment of more CCR7+dendritic cells (DCs) and lymphocytes into both RDLNs and spleen, resulting in a systemic lymphocyte expansion. Injury-induced intrarenal inflammation and fibrosis could be attenuated by blocking the recruitment of CCR7+cells into RDLN and spleen or inhibiting lymphangiogenesis. Elucidating the role of lymphangiogenesis in promoting intrarenal inflammation and fibrosis provides a key insight that can facilitate the development of novel therapeutic strategies to prevent progression of CKD-associated fibrosis.


1998 ◽  
Vol 30 (3) ◽  
pp. 377-382 ◽  
Author(s):  
Yoshihiko Sawa ◽  
Shigemitsu Yoshida ◽  
Yuichi Ashikaga ◽  
Takenori Kim ◽  
Yuji Yamaoka ◽  
...  

2006 ◽  
Vol 34 (6) ◽  
pp. 1002-1004 ◽  
Author(s):  
C.S. McKimmie ◽  
G.J. Graham

Selective sequestration of inflammatory chemokines is critical for the successful resolution of inflammatory responses in vivo. D6 is an atypical chemokine receptor that scavenges inflammatory chemokines and is pivotal in resolving models of chemokine-driven cutaneous inflammation. We provide evidence that expression of D6 is not limited to the lymphatic endothelium at sites of inflammation as previously believed. Instead we postulate that D6 expression in leucocytes may have a significant impact upon chemokine bioavailability during the resolution phase of inflammation. D6 expressed on the lymphatic endothelia may instead have complementary roles in preventing inappropriate leucocyte migration to the lymph node by keeping the endothelium free from inflammatory chemokines.


2000 ◽  
Vol 30 (1) ◽  
pp. 327-334 ◽  
Author(s):  
Alan J. Young ◽  
Tim J. Seabrook ◽  
Wendy L. Marston ◽  
Lisbeth Dudler ◽  
John B. Hay

Sign in / Sign up

Export Citation Format

Share Document