VEGF189 stimulates endothelial cells proliferation and migration in vitro and up-regulates the expression of Flk-1/KDR mRNA

2005 ◽  
Vol 309 (1) ◽  
pp. 24-31 ◽  
Author(s):  
Marie-Astrid Hervé ◽  
Hélène Buteau-Lozano ◽  
Samia Mourah ◽  
Fabien Calvo ◽  
Martine Perrot-Applanat
Keyword(s):  
Endothelial Cells ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Isolation and Characterisation of Lymphatic Endothelial Cells from Lung Tissues Affected by Lymphangioleiomyomatosis

2021 ◽  
Author(s):  
Koichi Nishino ◽  
Yasuhiro Yoshimatsu ◽  
Tomoki Muramatsu ◽  
Yasuhito Sekimoto ◽  
Keiko Mitani ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Normal Lung ◽  
Vascular Endothelial ◽  
Lymphatic Endothelial Cells ◽  
And Migration ◽  
Endothelial Growth Factor ◽  
Proliferation And Migration

Abstract Lymphangioleiomyomatosis (LAM) is a rare pulmonary disease characterised by the proliferation of smooth muscle-like cells (LAM cells), and an abundance of lymphatic vessels in LAM lesions. Studies reported that vascular endothelial growth factor-D (VEGF-D) secreted by LAM cells contributes to LAM-associated lymphangiogenesis, however, the precise mechanisms of lymphangiogenesis and characteristics of lymphatic endothelial cells (LECs) in LAM lesions have not yet been elucidated. In this study, human primary-cultured LECs were obtained both from LAM-affected lung tissues (LAM-LECs) and normal lung tissues (control LECs) using fluorescence-activated cell sorting (FACS). We found that LAM-LECs had significantly higher ability of proliferation and migration compared to control LECs. VEGF-D significantly promoted migration of LECs but not proliferation of LECs in vitro. cDNA microarray and FACS analysis revealed the expression of vascular endothelial growth factor receptor (VEGFR)-3 and integrin α9 were elevated in LAM-LECs. Inhibition of VEGFR-3 suppressed proliferation and migration of LECs, and blockade of integrin α9 reduced VEGF-D-induced migration of LECs. Our data uncovered the distinct features of LAM-associated LECs, increased proliferation and migration, which may be due to higher expression of VEGFR-3 and integrin α9. Furthermore, we also found VEGF-D/VEGFR-3 and VEGF-D/ integrin α9 signaling play an important role in LAM-associated lymphangiogenesis.

The Effect of Antiamoebic Agents on Viability, Proliferation and Migration of Human Epithelial Cells, Keratocytes and Endothelial Cells, In Vitro

2018 ◽  
Vol 43 (6) ◽  
pp. 725-733 ◽  
Author(s):  
Lei Shi ◽  
Tanja Stachon ◽  
Berthold Seitz ◽  
Stefan Wagenpfeil ◽  
Achim Langenbucher ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Epithelial Cells ◽  
Human Epithelial Cells ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Multivalent conjugates of basic fibroblast growth factor enhance in vitro proliferation and migration of endothelial cells

2018 ◽  
Vol 6 (5) ◽  
pp. 1076-1083 ◽  
Author(s):  
Aline Zbinden ◽  
Shane Browne ◽  
Eda I. Altiok ◽  
Felicia L. Svedlund ◽  
Wesley M. Jackson ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Great Promise ◽  
Fibroblast Growth ◽  
In Vitro Proliferation ◽  
And Migration ◽  
Regenerative Therapies ◽  
Proliferation And Migration

Multivalent growth factor conjugates hold great promise for regenerative therapies.

Tumour growth inhibition and anti-angiogenic effects using curcumin correspond to combined PDE2 and PDE4 inhibition

2015 ◽  
Vol 113 (02) ◽  
pp. 319-328 ◽  
Author(s):  
Abdurazzag Abusnina ◽  
Thérèse Keravis ◽  
Qingwei Zhou ◽  
Hélène Justiniano ◽  
Annelise Lobstein ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tumour Growth ◽  
Umbilical Vein ◽  
Camp Level ◽  
Pde4 Inhibitor ◽  
Endothelial Cell Proliferation ◽  
And Migration ◽  
Proliferation And Migration

SummaryVascular endothelial growth factor (VEGF) plays a major role in angiogenesis by stimulating endothelial cells. Increase in cyclic AMP (cAMP) level inhibits VEGF-induced endothelial cell proliferation and migration. Cyclic nucleotide phosphodiesterases (PDEs), which specifically hydrolyse cyclic nucleotides, are critical in the regulation of this signal transduction. We have previously reported that PDE2 and PDE4 up-regulations in human umbilical vein endothelial cells (HUVECs) are implicated in VEGF-induced angiogenesis and that inhibition of PDE2 and PDE4 activities prevents the development of the in vitro angiogenesis by increasing cAMP level, as well as the in vivo chicken embryo angiogenesis. We have also shown that polyphenols are able to inhibit PDEs. The curcumin having anti-cancer properties, the present study investigated whether PDE2 and PDE4 inhibitors and curcumin could have similar in vivo anti-tumour properties and whether the anti-angiogenic effects of curcumin are mediated by PDEs. Both PDE2/PDE4 inhibitor association and curcumin significantly inhibited in vivo tumour growth in C57BL/6N mice. In vitro, curcumin inhibited basal and VEGF-stimulated HUVEC proliferation and migration and delayed cell cycle progression at G0/G1, similarly to the combination of selective PDE2 and PDE4 inhibitors. cAMP levels in HUVECs were significantly increased by curcumin, similarly to rolipram (PDE4 inhibitor) and BAY-60–550 (PDE2 inhibitor) association, indicating cAMP-PDE inhibitions. Moreover, curcumin was able to inhibit VEGF-induced cAMP-PDE activity without acting on cGMP-PDE activity and to modulate PDE2 and PDE4 expressions in HUVECs. The present results suggest that curcumin exerts its in vitro anti-angiogenic and in vivo antitumour properties through combined PDE2 and PDE4 inhibition.

Adenosine and hypoxia stimulate proliferation and migration of endothelial cells

1988 ◽  
Vol 255 (3) ◽  
pp. H554-H562 ◽  
Author(s):  
C. J. Meininger ◽  
M. E. Schelling ◽  
H. J. Granger
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cells ◽  
Culture Medium ◽  
Culture Conditions ◽  
Hypoxic Conditions ◽  
Cell Counts ◽  
And Migration ◽  
Stimulate Cell Proliferation ◽  
Proliferation And Migration

The proliferation of bovine aortic or coronary venular endothelial cells (EC) in vitro was stimulated by the addition of adenosine (0.5 or 5.0 microM) to the culture medium. Cell counts of adenosine-treated aortic EC were 23–76% and coronary venular EC 19–52% greater than nontreated controls. Because adenosine is known to be released by hypoxic tissues, cell proliferation was quantitated when aortic EC were grown at 2% O2. Cell counts were 41–102% greater under hypoxic conditions than when cells were grown at standard tissue culture conditions (approximately 20% O2). When culture medium conditioned by coronary EC grown at 2% O2 was added to EC growing at standard conditions, cell counts were 24–69% greater than controls with medium conditioned by coronary EC grown at 20% O2. This suggests that hypoxia causes endothelial cells to release a factor(s) into the medium that can stimulate cell proliferation. The addition of the adenosine receptor blocker 8-phenyltheophylline (10(-5) M) prevented the stimulation of proliferation caused by hypoxia-conditioned medium, 2% O2 or 5.0 microM adenosine, suggesting that adenosine mediates its effect via an external membrane receptor. Adenosine also stimulated EC chemotaxis. Taken together, these results suggest that adenosine, released as a result of tissue hypoxia, may act as an angiogenic stimulus for the growth of new blood vessels.

scholarly journals Identification of Key Genes Associated with Endothelial Cell Dysfunction in Atherosclerosis Using Multiple Bioinformatics Tools

2022 ◽  
Vol 2022 ◽  
pp. 1-22
Author(s):  
Guofu Zhang ◽  
Hui Yu ◽  
Jingjing Su ◽  
Chao Chi ◽  
Lide Su ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Network Analysis ◽  
Endothelial Cell Dysfunction ◽  
Gene Set ◽  
Cell Dysfunction ◽  
Key Genes ◽  
And Migration ◽  
Proliferation And Migration

Atherosclerosis is the most notable cardiovascular disease, the latter being the main cause of death globally. Endothelial cell dysfunction plays a major role in the pathogenesis of atherosclerosis. However, it is currently unclear which genes are involved between endothelial cell dysfunction and atherosclerosis. This study was aimed at identifying these genes. Based on the GSE83500 dataset, the quantification of endothelial cell function was conducted using single-sample gene set enrichment analysis; the coexpression modules were conducted using weighted correlation network analysis. After building module-trait relationships, tan and yellow modules were regarded as hub modules. 10 hub genes from each hub module were identified by the protein-protein interaction network analysis. The key genes (RAB5A, CTTN, ITGB1, and MMP9) were obtained by comparing the expression differences of the hub gene between atherosclerotic and normal groups from the GSE28829 and GSE43292 datasets, respectively. ROC analysis showed the diagnostic value of key genes. Moreover, the differential expression of key genes in normal and atherosclerotic aortic walls was verified. In vitro, we establish a model of ox-LDL-injured endothelial cells and transfect RAB5A overexpression and shRNA plasmids. The results showed that overexpression of RAB5A ameliorates the proliferation and migration function of ox-LDL-injured endothelial cells, including the ability of tubule formation. It was speculated that the interferon response, Notch signaling pathways, etc. were involved in this function of RAB5A by using gene set variation analysis. With the multiple bioinformatics analysis methods, we detected that yellow and tan modules are related to the abnormal proliferation and migration of endothelial cells associated with atherosclerosis. RAB5A, CTTN, ITGB1, and MMP9 can be used as potential targets for therapy and diagnostic markers. In vitro, overexpression of RAB5A can ameliorate the proliferation and migration function of ox-LDL-injured endothelial cells, and the possible molecules involved in this process were speculated.

Macroporous methacrylated hyaluronic acid hydrogel with different pore sizes for in vitro and in vivo evaluation of vascularization

2022 ◽  
Author(s):  
Daohuan Lu ◽  
Zhiwen Zeng ◽  
Zhijie Geng ◽  
Cuiping Guo ◽  
Dating Pei ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Hyaluronic Acid ◽  
Pore Size ◽  
Umbilical Vein ◽  
Gelatin Microspheres ◽  
Pore Sizes ◽  
And Migration ◽  
Proliferation And Migration

Abstract Vascularization of thick hydrogel scaffolds is still a big challenge, because the submicron- or nano-sized pores seriously restrict endothelial cells adhesion, proliferation and migration. Therefore, porous hydrogels have been fabricated as a kind of promising hydrous scaffolds for enhancing vascularization during tissue repairing. In order to investigate the effects of pore size on vascularization, macroporous methacrylated hyaluronic acid (HAMA) hydrogels with different pore sizes were fabricated by a gelatin microspheres (GMS) template method. After leaching out GMS templates, uniform and highly interconnected macropores were formed in hydrogels, which provided an ideal physical microenvironment to induce human umbilical vein endothelial cells (HUVECs) migration and tissue vascularization. In vitro results revealed that macroporous hydrogels facilitated cells proliferation and migration compared with non-macroporous hydrogels. Hydrogels with middle pore size of 200-250 μm (HAMA250 hydrogels) supported the best cell proliferation and furthest 3D migration of HUVECs. The influences of pore sizes on vascularization were then evaluated with subcutaneous embedding. In vivo results illustrated that HAMA250 hydrogels exhibited optimum vascularization behavior. Highest number of newly formed blood vessels and expression of CD31 could be found in HAMA250 hydrogels rather than in other hydrogels. In summary, our results concluded that the best pore size for endothelial cells migration and tissue vascularization was 200-250 μm. This research provides a new insight into the engineering vascularized tissues and may find utility in designing regenerative biomaterial scaffolds

scholarly journals Isolation and characterisation of lymphatic endothelial cells from lung tissues affected by lymphangioleiomyomatosis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Koichi Nishino ◽  
Yasuhiro Yoshimatsu ◽  
Tomoki Muramatsu ◽  
Yasuhito Sekimoto ◽  
Keiko Mitani ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Normal Lung ◽  
Vascular Endothelial ◽  
Lymphatic Endothelial Cells ◽  
And Migration ◽  
Endothelial Growth Factor ◽  
Proliferation And Migration

AbstractLymphangioleiomyomatosis (LAM) is a rare pulmonary disease characterised by the proliferation of smooth muscle-like cells (LAM cells), and an abundance of lymphatic vessels in LAM lesions. Studies reported that vascular endothelial growth factor-D (VEGF-D) secreted by LAM cells contributes to LAM-associated lymphangiogenesis, however, the precise mechanisms of lymphangiogenesis and characteristics of lymphatic endothelial cells (LECs) in LAM lesions have not yet been elucidated. In this study, human primary-cultured LECs were obtained both from LAM-affected lung tissues (LAM-LECs) and normal lung tissues (control LECs) using fluorescence-activated cell sorting (FACS). We found that LAM-LECs had significantly higher ability of proliferation and migration compared to control LECs. VEGF-D significantly promoted migration of LECs but not proliferation of LECs in vitro. cDNA microarray and FACS analysis revealed the expression of vascular endothelial growth factor receptor (VEGFR)-3 and integrin α9 were elevated in LAM-LECs. Inhibition of VEGFR-3 suppressed proliferation and migration of LECs, and blockade of integrin α9 reduced VEGF-D-induced migration of LECs. Our data uncovered the distinct features of LAM-associated LECs, increased proliferation and migration, which may be due to higher expression of VEGFR-3 and integrin α9. Furthermore, we also found VEGF-D/VEGFR-3 and VEGF-D/ integrin α9 signaling play an important role in LAM-associated lymphangiogenesis.

Platelet-Derived Exosomes Affect the Proliferation and Migration of Human Umbilical Vein Endothelial Cells Via miR-126

2019 ◽  
Vol 17 (4) ◽  
pp. 379-387 ◽  
Author(s):  
Yan Sun ◽  
Xiao-li Liu ◽  
Dai Zhang ◽  
Fang Liu ◽  
Yu-jing Cheng ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Real Time ◽  
Umbilical Vein ◽  
Angiogenic Factors ◽  
Healthy Donors ◽  
And Migration ◽  
Umbilical Vein Endothelial Cells ◽  
Tgf Β1 ◽  
Proliferation And Migration

Background:Intraplaque angiogenesis, the process of generating new blood vessels mediated by endothelial cells, contributes to plaque growth, intraplaque hemorrhage, and thromboembolic events. Platelet-derived Exosomes (PLT-EXOs) affect angiogenesis in multiple ways. The ability of miR-126, one of the best-characterized miRNAs that regulates angiogenesis, carried by PLT-EXOs to influence angiogenesis via the regulation of the proliferation and migration of endothelial cells is unknown. In this study, we aimed to investigate the effects of PLT-EXOs on angiogenesis by Human Umbilical Vein Endothelial Cells (HUVECs).Methods:We evaluated the levels of miR-126 and angiogenic factors in PLT-EXOs from Acute Coronary Syndrome (ACS) patients and healthy donors by real-time Polymerase Chain Reaction (PCR) and western blotting. We incubated HUVECs with PLT-EXOs and measured cell proliferation and migration with the Cell Counting Kit-8 assay and scratch assay, respectively. We also investigated the expression of miR-126 and angiogenic factors in HUVECs after exposure to PLT-EXOs by western blotting and real-time PCR.Results:PLT-EXOs from ACS patients contained higher levels of miR-126 and angiogenic factors, including Vascular Endothelial Growth Factor (VEGF), basic Fibroblast Growth Factor (bFGF), and Transforming Growth Factor Beta 1 (TGF-β1), than those from healthy donors (p<0.05). Moreover, the levels of exosomal miR-126 and angiogenic factors were increased after stimulation with thrombin (p<0.01). HUVEC proliferation and migration were promoted by treatment with activated PLT-EXOs (p<0.01); they were accompanied by the over-expression of miR-126 and angiogenic factors, including VEGF, bFGF, and TGF-β1 (p<0.01).Conclusion:Activated PLT-EXOs promoted the proliferation and migration of HUVECs, and the overexpression of miR-126 and angiogenic factors, thereby elucidating potential new therapeutic targets for intraplaque angiogenesis.

scholarly journals Hypoxic glioma-derived exosomes promote M2-like macrophage polarization by enhancing autophagy induction

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Jianye Xu ◽  
Jian Zhang ◽  
Zongpu Zhang ◽  
Zijie Gao ◽  
Yanhua Qi ◽  
...  
Keyword(s):  
Macrophage Polarization ◽  
Autophagy Induction ◽  
Antitumor Immunotherapy ◽  
Novel Biomarkers ◽  
And Migration ◽  
Immunosuppressive Microenvironment ◽  
Proliferation And Migration ◽  
Glioma Progression

AbstractExosomes participate in intercellular communication and glioma microenvironment modulation, but the exact mechanisms by which glioma-derived exosomes (GDEs) promote the generation of the immunosuppressive microenvironment are still unclear. Here, we investigated the effects of GDEs on autophagy, the polarization of tumor-associated macrophages (TAMs), and glioma progression. Compared with normoxic glioma-derived exosomes (N-GDEs), hypoxic glioma-derived exosomes (H-GDEs) markedly facilitated autophagy and M2-like macrophage polarization, which subsequently promoted glioma proliferation and migration in vitro and in vivo. Western blot and qRT-PCR analyses indicated that interleukin 6 (IL-6) and miR-155-3p were highly expressed in H-GDEs. Further experiments showed that IL-6 and miR-155-3p induced M2-like macrophage polarization via the IL-6-pSTAT3-miR-155-3p-autophagy-pSTAT3 positive feedback loop, which promotes glioma progression. Our study clarifies a mechanism by which hypoxia and glioma influence autophagy and M2-like macrophage polarization via exosomes, which could advance the formation of the immunosuppressive microenvironment. Our findings suggest that IL-6 and miR-155-3p may be novel biomarkers for diagnosing glioma and that treatments targeting autophagy and the STAT3 pathway may contribute to antitumor immunotherapy.

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