scholarly journals The impact of chronic intermittent hypoxia on the expression of intercellular cell adhesion molecule-1 and vascular endothelial growth factor in the ischemia-reperfusion rat model

2018 ◽  
Vol 56 (3) ◽  
pp. 159-166 ◽  
Author(s):  
Meili Yang ◽  
Yafang Chen ◽  
Zhengang Wu ◽  
Yaping Zhang ◽  
Ruowei Cai ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Intermittent Hypoxia ◽  
Cell Adhesion Molecule ◽  
Ischemia Reperfusion ◽  
Chronic Intermittent Hypoxia ◽  
Vascular Endothelial ◽  
Cell Adhesion Molecule 1 ◽  
Endothelial Growth Factor ◽  
The Impact ◽  
Intercellular Cell Adhesion Molecule

scholarly journals Recombinant vascular endothelial growth factor 121 decreases vascular cell adhesion molecule-1 in murine pre-eclampsia model placenta

2016 ◽  
Vol 35 (3) ◽  
pp. 192
Author(s):  
Sri Sulistyowati ◽  
John Arianto Sondakh ◽  
Eric Edwin Yuliantara ◽  
Supriyadi Hari Respati ◽  
Soetrisno Soetrisno
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cell Adhesion Molecule ◽  
Angiogenic Factor ◽  
Vascular Endothelial ◽  
Vascular Cell Adhesion ◽  
Vascular Cell ◽  
Pregnant Mice ◽  
Cell Adhesion Molecule 1 ◽  
Endothelial Growth Factor

Background<br />Preeclampsia is one of the major contributors to maternal and fetal morbidity and mortality. Imbalance of soluble Fms-like tyrosine kinase (sFlt-1) as anti-angiogenic factor and vascular endothelial growth factor (VEGF) as pro-angiogenic factor plays a role in the pathogenesis of preeclampsia. Endothelial dysfunction in preeclampsia causes vascular cell adhesion molecule-1 (VCAM-1) to be expressed on its surface. This study aims to evaluate the effect of recombinant VEGF-121 on VCAM-1 expression in the placenta of a murine preeclampsia model. <br /><br />Methods <br />An experimental analytical study conducted from February until March 2016 in the Biomedical Laboratory, Faculty of Veterinary Medicine, Airlangga University. The study sample consisted of 30 pregnant mice, divided into three groups, i.e. 10 normal pregnant mice, 10 mice with preeclampsia model and 10 mice with preeclampsia model and recombinant VEGF-121 therapy. All animals were subjected to immunohistochemical examination of VCAM-1 expression in their placentas. The results were assessed semiquantitatively according to a modified Remmele method. Data analysis was done using one-way ANOVA and Tukey’s multiple comparisons method. <br /><br />Results<br />Mean VCAM-1 expression in normal (0.97 ± 0.54%) murine placentas, compared with placentas (2.94 ± 0.96%) of murine preeclampsia models (p=0.000), while mean VCAM-1 expression in placentas of murine preeclampsia models with VEGF intervention was 2.14 ± 0.68% (p=0.030).<br /><br />Conclusion <br />Recombinant VEGF-121 can reduce VCAM-1 expression in placentas of murine preeclampsia models. The present study has shown the potential benefits of VEGF therapy, justifying serious consideration of this therapeutic approach for use in women with preeclampsia.

Lymphatic reprogramming of microvascular endothelial cells by CEA-related cell adhesion molecule-1 via interaction with VEGFR-3 and Prox1

Blood ◽  
2007 ◽  
Vol 110 (13) ◽  
pp. 4223-4233 ◽  
Author(s):  
Nerbil Kilic ◽  
Leticia Oliveira-Ferrer ◽  
Samira Neshat-Vahid ◽  
Ster Irmak ◽  
Kirstin Obst-Pernberg ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Growth Factor ◽  
Cell Adhesion Molecule ◽  
Microvascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Tyrosine Residues ◽  
Related Cell ◽  
Cell Adhesion Molecule 1 ◽  
Endothelial Growth Factor

Here, we demonstrate that carcinoembryonic antigen-related cell adhesion molecule-1 (CEACAM1) is expressed and co-localized with podoplanin in lymphatic endothelial cells (LECs) of tumor but not of normal tissue. CEACAM1 overexpression in human dermal microvascular endothelial cells (HDMECs) results in a significant increase of podoplanin-positive cells in fluorescence-activated cell sorting analyses, while such effects are not observed in CEACAM1 overexpressing human umbilical vein endothelial cell (HUVECs). This effect of CEACAM1 is ceased when HDMECs are transfected with CEACAM1/y− missing the tyrosine residues in its cytoplasmic domain. CEACAM1 overexpression in HDMECs leads to an up-regulation of vascular endothelial growth factor C, -D (VEGF-C, -D) and their receptor vascular endothelial growth factor receptor 3 (VEGFR-3) at mRNA and protein levels. HDMECs transfected with CEACAM1 but not those with CEACAM1/y− show enhanced expression of the lymphatic markers Prox1, podoplanin, and LYVE-1. Furthermore, Prox1 silencing in HDMECs via small interfering RNA blocks the CEACAM1-induced increase of VEGFR-3 expression. Number and network of endothelial tubes induced by VEGF-C and -D are enhanced in CEACAM1-overexpressing HDMECs. Moreover, VEGF-A treatment of CEACAM1-silenced HDMECs restores their survival but not that with VEGF-C and VEGF-D. These data imply that the interaction of CEACAM1 with Prox1 and VEGFR-3 plays a crucial role in tumor lymphangiogenesis and reprogramming of vascular endothelial cells to LECs. CEACAM1-induced signaling effects appear to be dependent on the presence of tyrosine residues in the CEACAM1 cytoplasmic domain.

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