Vascular endothelial growth factor C is increased in endometrium and promotes endothelial functions, vascular permeability and angiogenesis and growth of endometriosis

Endometriosis is an angiogenesis-dependent disease. Many studies demonstrated inhibition of angiogenesis leads to inhibition of endometriotic growth, however underlying mechanism is still not fully understood. Our previous study suggested vascular endothelial growth factor C (VEGF-C) as a target of...

Full description

Bibliographic Details
Main Authors: Xu, H, Zhang, T, Man, G, May, K, Becker, C, Davis, T, Kung, A, Birsner, A, D'Amato, R, Wong, A, Wang, C
Format: Journal article
Language:English
Published: 2013
_version_ 1797105184534429696
author Xu, H
Zhang, T
Man, G
May, K
Becker, C
Davis, T
Kung, A
Birsner, A
D'Amato, R
Wong, A
Wang, C
author_facet Xu, H
Zhang, T
Man, G
May, K
Becker, C
Davis, T
Kung, A
Birsner, A
D'Amato, R
Wong, A
Wang, C
author_sort Xu, H
collection OXFORD
description Endometriosis is an angiogenesis-dependent disease. Many studies demonstrated inhibition of angiogenesis leads to inhibition of endometriotic growth, however underlying mechanism is still not fully understood. Our previous study suggested vascular endothelial growth factor C (VEGF-C) as a target of anti-angiogenesis therapy for endometriosis. In this study, VEGF-C in endometrium and its role in angiogenesis of endometriosis were studied. Human endometrium were obtained from women with and without endometriosis for molecular studies. VEGF-A, VEGF-B, VEGF-C and VEGF-D mRNA and proteins in eutopic and ectopic endometrium were measured. Human endothelial cells were transfected with VEGF-C siRNA in vitro, effects of VEGF-C on endothelial cell migration, invasion and tube formation were investigated in vitro. Angiogenesis was inhibited in wild type mice, vascular permeability in dermal skin was determined in vivo. Transplanted endometrium were inhibited by VEGF-C siRNA in immunocompromised mice, development, growth and angiogenesis of the experimental endometriosis were compared in vivo. The results showed that VEGF-C mRNA and protein were increased in eutopic and ectopic endometrium of endometriosis patients. VEGF-C siRNA significantly inhibited endothelial cell migration and tube formation. VEGF-C siRNA significantly inhibited development and angiogenesis of the experimental endometriotic lesions in mice. Supplementation and over-expression of VEGF-C significantly reversed the inhibitory effects on the endothelial functions, vascular permeability and endometriotic growth. In conclusion, VEGF-C is increased in endometrium and it promotes endothelial functions, vascular permeability and development of experimental endometriosis. VEGF-C is important for angiogenesis in endometriosis. © 2013 Springer Science+Business Media Dordrecht.
first_indexed 2024-03-07T06:43:51Z
format Journal article
id oxford-uuid:fa367a86-5f9d-4b78-a2b7-eab7e1b7804d
institution University of Oxford
language English
last_indexed 2024-03-07T06:43:51Z
publishDate 2013
record_format dspace
spelling oxford-uuid:fa367a86-5f9d-4b78-a2b7-eab7e1b7804d2022-03-27T13:03:57ZVascular endothelial growth factor C is increased in endometrium and promotes endothelial functions, vascular permeability and angiogenesis and growth of endometriosisJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:fa367a86-5f9d-4b78-a2b7-eab7e1b7804dEnglishSymplectic Elements at Oxford2013Xu, HZhang, TMan, GMay, KBecker, CDavis, TKung, ABirsner, AD'Amato, RWong, AWang, CEndometriosis is an angiogenesis-dependent disease. Many studies demonstrated inhibition of angiogenesis leads to inhibition of endometriotic growth, however underlying mechanism is still not fully understood. Our previous study suggested vascular endothelial growth factor C (VEGF-C) as a target of anti-angiogenesis therapy for endometriosis. In this study, VEGF-C in endometrium and its role in angiogenesis of endometriosis were studied. Human endometrium were obtained from women with and without endometriosis for molecular studies. VEGF-A, VEGF-B, VEGF-C and VEGF-D mRNA and proteins in eutopic and ectopic endometrium were measured. Human endothelial cells were transfected with VEGF-C siRNA in vitro, effects of VEGF-C on endothelial cell migration, invasion and tube formation were investigated in vitro. Angiogenesis was inhibited in wild type mice, vascular permeability in dermal skin was determined in vivo. Transplanted endometrium were inhibited by VEGF-C siRNA in immunocompromised mice, development, growth and angiogenesis of the experimental endometriosis were compared in vivo. The results showed that VEGF-C mRNA and protein were increased in eutopic and ectopic endometrium of endometriosis patients. VEGF-C siRNA significantly inhibited endothelial cell migration and tube formation. VEGF-C siRNA significantly inhibited development and angiogenesis of the experimental endometriotic lesions in mice. Supplementation and over-expression of VEGF-C significantly reversed the inhibitory effects on the endothelial functions, vascular permeability and endometriotic growth. In conclusion, VEGF-C is increased in endometrium and it promotes endothelial functions, vascular permeability and development of experimental endometriosis. VEGF-C is important for angiogenesis in endometriosis. © 2013 Springer Science+Business Media Dordrecht.
spellingShingle Xu, H
Zhang, T
Man, G
May, K
Becker, C
Davis, T
Kung, A
Birsner, A
D'Amato, R
Wong, A
Wang, C
Vascular endothelial growth factor C is increased in endometrium and promotes endothelial functions, vascular permeability and angiogenesis and growth of endometriosis
title Vascular endothelial growth factor C is increased in endometrium and promotes endothelial functions, vascular permeability and angiogenesis and growth of endometriosis
title_full Vascular endothelial growth factor C is increased in endometrium and promotes endothelial functions, vascular permeability and angiogenesis and growth of endometriosis
title_fullStr Vascular endothelial growth factor C is increased in endometrium and promotes endothelial functions, vascular permeability and angiogenesis and growth of endometriosis
title_full_unstemmed Vascular endothelial growth factor C is increased in endometrium and promotes endothelial functions, vascular permeability and angiogenesis and growth of endometriosis
title_short Vascular endothelial growth factor C is increased in endometrium and promotes endothelial functions, vascular permeability and angiogenesis and growth of endometriosis
title_sort vascular endothelial growth factor c is increased in endometrium and promotes endothelial functions vascular permeability and angiogenesis and growth of endometriosis
work_keys_str_mv AT xuh vascularendothelialgrowthfactorcisincreasedinendometriumandpromotesendothelialfunctionsvascularpermeabilityandangiogenesisandgrowthofendometriosis
AT zhangt vascularendothelialgrowthfactorcisincreasedinendometriumandpromotesendothelialfunctionsvascularpermeabilityandangiogenesisandgrowthofendometriosis
AT mang vascularendothelialgrowthfactorcisincreasedinendometriumandpromotesendothelialfunctionsvascularpermeabilityandangiogenesisandgrowthofendometriosis
AT mayk vascularendothelialgrowthfactorcisincreasedinendometriumandpromotesendothelialfunctionsvascularpermeabilityandangiogenesisandgrowthofendometriosis
AT beckerc vascularendothelialgrowthfactorcisincreasedinendometriumandpromotesendothelialfunctionsvascularpermeabilityandangiogenesisandgrowthofendometriosis
AT davist vascularendothelialgrowthfactorcisincreasedinendometriumandpromotesendothelialfunctionsvascularpermeabilityandangiogenesisandgrowthofendometriosis
AT kunga vascularendothelialgrowthfactorcisincreasedinendometriumandpromotesendothelialfunctionsvascularpermeabilityandangiogenesisandgrowthofendometriosis
AT birsnera vascularendothelialgrowthfactorcisincreasedinendometriumandpromotesendothelialfunctionsvascularpermeabilityandangiogenesisandgrowthofendometriosis
AT damator vascularendothelialgrowthfactorcisincreasedinendometriumandpromotesendothelialfunctionsvascularpermeabilityandangiogenesisandgrowthofendometriosis
AT wonga vascularendothelialgrowthfactorcisincreasedinendometriumandpromotesendothelialfunctionsvascularpermeabilityandangiogenesisandgrowthofendometriosis
AT wangc vascularendothelialgrowthfactorcisincreasedinendometriumandpromotesendothelialfunctionsvascularpermeabilityandangiogenesisandgrowthofendometriosis