CXCL12 enhances angiogenesis through CXCR7 activation in human umbilical vein endothelial cells

Abstract Angiogenesis is the process by which new vessels form from existing vascular networks. Human umbilical vein endothelial cells (HUVECs) may contribute to the study of vascular repair and angiogenesis. The chemokine CXCL12 regulates multiple cell functions, including angiogenesis, mainly thro...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Min Zhang, Lisha Qiu, Yanyan Zhang, Dongsheng Xu, Jialin C. Zheng, Li Jiang
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2017
Materias:
R
Q
Acceso en línea:https://doaj.org/article/d7352edfa3f743dfacbb77c34bfc3a60
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:d7352edfa3f743dfacbb77c34bfc3a60
record_format dspace
spelling oai:doaj.org-article:d7352edfa3f743dfacbb77c34bfc3a602021-12-02T15:05:24ZCXCL12 enhances angiogenesis through CXCR7 activation in human umbilical vein endothelial cells10.1038/s41598-017-08840-y2045-2322https://doaj.org/article/d7352edfa3f743dfacbb77c34bfc3a602017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-08840-yhttps://doaj.org/toc/2045-2322Abstract Angiogenesis is the process by which new vessels form from existing vascular networks. Human umbilical vein endothelial cells (HUVECs) may contribute to the study of vascular repair and angiogenesis. The chemokine CXCL12 regulates multiple cell functions, including angiogenesis, mainly through its receptor CXCR4. In contrast to CXCL12/CXCR4, few studies have described roles for CXCR7 in vascular biology, and the downstream mechanism of CXCR7 in angiogenesis remains unclear. The results of the present study showed that CXCL12 dose-dependently enhanced angiogenesis in chorioallantoic membranes (CAMs) and HUVECs. The specific activation of CXCR7 with TC14012 (a CXCR7 agonist) resulted in the significant induction of tube formation in HUVECs and in vivo. Further evidence suggested that CXCL12 induced directional polarization and migration in the HUVECs, which is necessary for tube formation. Moreover, CXCR7 translocalization was observed during the polarization of HUVECs in stripe assays. Finally, treatment with TC14012 also significantly increased PI3K/Akt phosphorylation, and tube formation was blocked by treating HUVECs with an Akt inhibitor. Overall, this study indicated that CXCL12-stimulated CXCR7 acts as a functional receptor to activate Akt for angiogenesis in HUVECs and that CXCR7 may be a potential target molecule for endothelial regeneration and repair after vascular injury.Min ZhangLisha QiuYanyan ZhangDongsheng XuJialin C. ZhengLi JiangNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-9 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Min Zhang
Lisha Qiu
Yanyan Zhang
Dongsheng Xu
Jialin C. Zheng
Li Jiang
CXCL12 enhances angiogenesis through CXCR7 activation in human umbilical vein endothelial cells
description Abstract Angiogenesis is the process by which new vessels form from existing vascular networks. Human umbilical vein endothelial cells (HUVECs) may contribute to the study of vascular repair and angiogenesis. The chemokine CXCL12 regulates multiple cell functions, including angiogenesis, mainly through its receptor CXCR4. In contrast to CXCL12/CXCR4, few studies have described roles for CXCR7 in vascular biology, and the downstream mechanism of CXCR7 in angiogenesis remains unclear. The results of the present study showed that CXCL12 dose-dependently enhanced angiogenesis in chorioallantoic membranes (CAMs) and HUVECs. The specific activation of CXCR7 with TC14012 (a CXCR7 agonist) resulted in the significant induction of tube formation in HUVECs and in vivo. Further evidence suggested that CXCL12 induced directional polarization and migration in the HUVECs, which is necessary for tube formation. Moreover, CXCR7 translocalization was observed during the polarization of HUVECs in stripe assays. Finally, treatment with TC14012 also significantly increased PI3K/Akt phosphorylation, and tube formation was blocked by treating HUVECs with an Akt inhibitor. Overall, this study indicated that CXCL12-stimulated CXCR7 acts as a functional receptor to activate Akt for angiogenesis in HUVECs and that CXCR7 may be a potential target molecule for endothelial regeneration and repair after vascular injury.
format article
author Min Zhang
Lisha Qiu
Yanyan Zhang
Dongsheng Xu
Jialin C. Zheng
Li Jiang
author_facet Min Zhang
Lisha Qiu
Yanyan Zhang
Dongsheng Xu
Jialin C. Zheng
Li Jiang
author_sort Min Zhang
title CXCL12 enhances angiogenesis through CXCR7 activation in human umbilical vein endothelial cells
title_short CXCL12 enhances angiogenesis through CXCR7 activation in human umbilical vein endothelial cells
title_full CXCL12 enhances angiogenesis through CXCR7 activation in human umbilical vein endothelial cells
title_fullStr CXCL12 enhances angiogenesis through CXCR7 activation in human umbilical vein endothelial cells
title_full_unstemmed CXCL12 enhances angiogenesis through CXCR7 activation in human umbilical vein endothelial cells
title_sort cxcl12 enhances angiogenesis through cxcr7 activation in human umbilical vein endothelial cells
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/d7352edfa3f743dfacbb77c34bfc3a60
work_keys_str_mv AT minzhang cxcl12enhancesangiogenesisthroughcxcr7activationinhumanumbilicalveinendothelialcells
AT lishaqiu cxcl12enhancesangiogenesisthroughcxcr7activationinhumanumbilicalveinendothelialcells
AT yanyanzhang cxcl12enhancesangiogenesisthroughcxcr7activationinhumanumbilicalveinendothelialcells
AT dongshengxu cxcl12enhancesangiogenesisthroughcxcr7activationinhumanumbilicalveinendothelialcells
AT jialinczheng cxcl12enhancesangiogenesisthroughcxcr7activationinhumanumbilicalveinendothelialcells
AT lijiang cxcl12enhancesangiogenesisthroughcxcr7activationinhumanumbilicalveinendothelialcells
_version_ 1718388860043395072