Galectin-8 Favors VEGF-Induced Angiogenesis: In Vitro Study in Human Umbilical Vein Endothelial Cells and In Vivo Study in Chick Chorioallantoic Membrane
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F20%3A00555715" target="_blank" >RIV/68378050:_____/20:00555715 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/00216208:11120/20:43920188
Výsledek na webu
<a href="https://ar.iiarjournals.org/content/40/6/3191" target="_blank" >https://ar.iiarjournals.org/content/40/6/3191</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.21873/anticanres.14300" target="_blank" >10.21873/anticanres.14300</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Galectin-8 Favors VEGF-Induced Angiogenesis: In Vitro Study in Human Umbilical Vein Endothelial Cells and In Vivo Study in Chick Chorioallantoic Membrane
Popis výsledku v původním jazyce
Background/Aim: Although it has been accepted that the tandem repeat galectin-8 (Gal-8) is linked to angiogenesis, the underlying mechanisms in endothelial cells has remained poorly understood. In this study we aimed to investigate the effect of Gal-8 on selected biological processes linked to angiogenesis in in vitro and in vivo models. Materials and Methods: In detail, we assessed how exogenously added human recombinant Gal-8 (with or without vascular endothelial growth factor VEGF) affects selected steps involved in vessel formation in human umbilical vein endothelial cells (HUVECs) as well as using the chick chorioallantoic membrane (CAM) assay. Gene expression profiling of HUVECs was performed to extend the scope of our investigation. Results: Our findings demonstrate that Gal-8 in combination with VEGF enhanced cell proliferation and migration, two cellular events linked to angiogenesis. However, Gal-8 alone did not exhibit any significant effects on cell proliferation or on cell migration. The molecular analysis revealed that Gal-8 in the presence of VEGF influenced cytokine-cytokine receptor interactions, HIF-1 and PI3K/AKT signaling pathways. Gal-8 alone also targeted cytokine-cytokine receptor interactions, but with a different expression profile as well as a modulated focal adhesion and TNF signaling. Conclusion: Gal-8 promotes a pro-angiogenic phenotype possibly in a synergistic manner with VEGF.
Název v anglickém jazyce
Galectin-8 Favors VEGF-Induced Angiogenesis: In Vitro Study in Human Umbilical Vein Endothelial Cells and In Vivo Study in Chick Chorioallantoic Membrane
Popis výsledku anglicky
Background/Aim: Although it has been accepted that the tandem repeat galectin-8 (Gal-8) is linked to angiogenesis, the underlying mechanisms in endothelial cells has remained poorly understood. In this study we aimed to investigate the effect of Gal-8 on selected biological processes linked to angiogenesis in in vitro and in vivo models. Materials and Methods: In detail, we assessed how exogenously added human recombinant Gal-8 (with or without vascular endothelial growth factor VEGF) affects selected steps involved in vessel formation in human umbilical vein endothelial cells (HUVECs) as well as using the chick chorioallantoic membrane (CAM) assay. Gene expression profiling of HUVECs was performed to extend the scope of our investigation. Results: Our findings demonstrate that Gal-8 in combination with VEGF enhanced cell proliferation and migration, two cellular events linked to angiogenesis. However, Gal-8 alone did not exhibit any significant effects on cell proliferation or on cell migration. The molecular analysis revealed that Gal-8 in the presence of VEGF influenced cytokine-cytokine receptor interactions, HIF-1 and PI3K/AKT signaling pathways. Gal-8 alone also targeted cytokine-cytokine receptor interactions, but with a different expression profile as well as a modulated focal adhesion and TNF signaling. Conclusion: Gal-8 promotes a pro-angiogenic phenotype possibly in a synergistic manner with VEGF.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
30204 - Oncology
Návaznosti výsledku
Projekt
—
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2020
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Anticancer Research
ISSN
0250-7005
e-ISSN
1791-7530
Svazek periodika
40
Číslo periodika v rámci svazku
6
Stát vydavatele periodika
GR - Řecká republika
Počet stran výsledku
11
Strana od-do
3191-3201
Kód UT WoS článku
000538104800019
EID výsledku v databázi Scopus
—