Lymphangiogenesis:<i>in vitro</i>and<i>in vivo</i>models

Bruyère, Françoise; Noël, Agnès

doi:10.1096/fj.09-132852

Cited by 87 publications

(43 citation statements)

References 188 publications

(213 reference statements)

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“…More understanding of molecular mechanisms underlying tumour lymphangiogenesis will provide new insights into the process of metastasis. However, the study of lymphangiogenesis has been impeded by the difficulties in isolating and propagating LECs from different organs [42,43]. To overcome the above limitations, we used a 'conditionally immortalized' line of human LECs, which transformed with hTERT and maintained their 'lymphatic' endothelial characteristics after repeated passages.…”

Section: Discussionmentioning

confidence: 99%

Adiponectin promotes VEGF-C-dependent lymphangiogenesis by inhibiting miR-27b through a CaMKII/AMPK/p38 signaling pathway in human chondrosarcoma cells

et al. 2016

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Chondrosarcoma is the second most frequently occurring type of bone malignancy characterized by distant metastatic propensity. Vascular endothelial growth factor-C (VEGF-C) is the major lymphangiogenic factor, and makes crucial contributions to tumour lymphangiogenesis and lymphatic metastasis. Adiponectin is a protein hormone secreted predominantly by differentiated adipocytes. In recent years, adiponectin has also been indicated as facilitating tumorigenesis, angiogenesis and metastasis. However, the effect of adiponectin on VEGF-C regulation and lymphangiogenesis in chondrosarcoma has remained largely a mystery. In the present study, we have shown a clinical correlation between adiponectin and VEGF-C, as well as tumour stage, in human chondrosarcoma tissues. We further demonstrated that adiponectin promoted VEGF-C expression and secretion in human chondrosarcoma cells. The conditioned medium from adiponectin-treated cells significantly induced tube formation and migration of human lymphatic endothelial cells. In addition, adiponectin knock down inhibited lymphangiogenesis in vitro and in vivo We also found that adiponectin-induced VEGF-C is mediated by the calmodulin-dependent protein kinase II (CaMKII), AMP-activated protein kinase (AMPK) and p38 signaling pathway. Furthermore, the expression of miR-27b was negatively regulated by adiponectin via the CaMKII, AMPK and p38 cascade. The present study is the first to describe the mechanism of adiponectin-promoted lymphangiogenesis by up-regulating VEGF-C expression in chondrosarcomas. Thus, adiponectin could serve as a therapeutic target in chondrosarcoma metastasis and lymphangiogenesis.

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Section: Discussionmentioning

confidence: 99%

Adiponectin promotes VEGF-C-dependent lymphangiogenesis by inhibiting miR-27b through a CaMKII/AMPK/p38 signaling pathway in human chondrosarcoma cells

et al. 2016

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“…Dissection of the corneal pannus may not necessarily remove all fibrovascular or lymphatic tissue predisposing the graft bed to high risk of graft rejection (body of evidence suggests new lymphatics stem from preexisting ones 15 ). This underscores the need for developing pretreatment modalities for high-risk graft beds with anti-lymphangiogenic therapeutic agents, such as bevacizumab, 8 to improve chances of graft survival.…”

Section: Ocular Immunology and Inflammationmentioning

confidence: 99%

Lymphangiogenesis May Play a Role in Cultivated Limbal Stem Cell Transplant Rejection

Zakaria¹,

Koppen

Berneman

et al. 2012

Ocular Immunology and Inflammation

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“…Lymphangiogenesis, the formation of new lymphatic vessels, occurs in several pathological conditions ssociated with chronic inflammation [123,124], including portal hypertensive enteropathy [84] and liver cirrhosis [81,82]. Inflammatory cells, through the secretion of stimulatory factor such as VEGF-C and TNF-α, can stimulate lymphatic endothelial cells [125][126][127] and consequently regulate gut lymphatic remodeling in portal hypertensive enteropathy.…”

Section: Splanchnic Interstitium Mesenteric Lymphatics and Peritoneamentioning

confidence: 99%

Portal hypertension-related inflammatory phenotypes: From a vitelline and amniotic point of view

Aller¹,

Arias²,

Prieto³

et al. 2012

ABB

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Prehepatic portal hypertension induces a splanchnic low-grade inflammatory response that could switch to high-grade inflammation with the development of severe and life-threatening complications when associated with chronic liver disease. The extraembryonic origin of the portal system maybe determines the regression to an extraembryonic phenotype, i.e., vitellogenic and amniotic, during the evolution of both types of portal hypertension. Thus, prehepatic portal hypertension, or compensated hypertension by portal vein ligation in the rat, is associated with molecular mechanisms related to vitellogenesis, where hepatic steatosis and splanchnic angiogenesis stand out. In turn, extrahepatic cholestasis in the rat induces intrahepatic portal hypertension, or decompensated hypertension, with ascites and hepatorenal syndrome. The splanchnic interstitium, the mesenteric lymphatic system, and the peritoneal mesothelium seem to create an inflammatory pathway that could have a key pathophysiological relevance in the production of ascites. The hypothetical comparison between the ascitic and the amniotic fluid also allows for translational investtigation. The induced regression of the splanchnic system to extraembryonic functions by portal hypertension highlights the great relevance of the extraembryonic structures even during post-natal life.

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Lymphangiogenesis:in vitroandin vivomodels

Cited by 87 publications

References 188 publications

Adiponectin promotes VEGF-C-dependent lymphangiogenesis by inhibiting miR-27b through a CaMKII/AMPK/p38 signaling pathway in human chondrosarcoma cells

Adiponectin promotes VEGF-C-dependent lymphangiogenesis by inhibiting miR-27b through a CaMKII/AMPK/p38 signaling pathway in human chondrosarcoma cells

Lymphangiogenesis May Play a Role in Cultivated Limbal Stem Cell Transplant Rejection

Portal hypertension-related inflammatory phenotypes: From a vitelline and amniotic point of view

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