Dysregulation of focal adhesion kinase upon Toxoplasma gondii infection facilitates parasite translocation across polarised primary brain endothelial cell monolayers

2019 ◽  
Vol 21 (9) ◽  
Author(s):  
Emily C. Ross ◽  
Gabriela C. Olivera ◽  
Antonio Barragan
Keyword(s):  
Endothelial Cell ◽  
Toxoplasma Gondii ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Brain Endothelial Cell ◽  
Cell Monolayers ◽  
Toxoplasma Gondii Infection

scholarly journals Candida albicans Expresses a Focal Adhesion Kinase-Like Protein That Undergoes Increased Tyrosine Phosphorylation upon Yeast Cell Adhesion to Vitronectin and the EA.hy 926 Human Endothelial Cell Line

2002 ◽  
Vol 70 (7) ◽  
pp. 3804-3815 ◽  
Author(s):  
Giorgio Santoni ◽  
Roberta Lucciarini ◽  
Consuelo Amantini ◽  
Jordan Jacobelli ◽  
Elisabetta Spreghini ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Candida Albicans ◽  
Cell Adhesion ◽  
Endothelial Cell ◽  
Yeast Cell ◽  
Focal Adhesion Kinase ◽  
Cell Line ◽  
Tyrosine Phosphorylation ◽  
Focal Adhesion ◽  
Human Endothelial Cell Line

ABSTRACT The signaling pathways triggered by adherence of Candida albicans to the host cells or extracellular matrix are poorly understood. We provide here evidence in C. albicans yeasts of a p105 focal adhesion kinase (Fak)-like protein (that we termed CaFak), antigenically related to the vertebrate p125Fak, and its involvement in integrin-like-mediated fungus adhesion to vitronectin (VN) and EA.hy 926 human endothelial cell line. Biochemical analysis with different anti-chicken Fak antibodies identified CaFak as a 105-kDa protein and immunofluorescence and cytofluorimetric analysis on permeabilized cells specifically stain C. albicans yeasts; moreover, confocal microscopy evidences CaFak as a cytosolic protein that colocalizes on the membrane with the integrin-like VN receptors upon yeast adhesion to VN. The protein tyrosine kinase (PTK) inhibitors genistein and herbimycin A strongly inhibited C. albicans yeast adhesion to VN and EA.hy 926 endothelial cells. Moreover, engagement of αvβ3 and αvβ5 integrin-like on C. albicans either by specific monoclonal antibodies or upon adhesion to VN or EA.hy 926 endothelial cells stimulates CaFak tyrosine phosphorylation that is blocked by PTK inhibitor. A role for CaFak in C. albicans yeast adhesion was also supported by the failure of VN to stimulate its tyrosine phosphorylation in a C. albicans mutant showing normal levels of CaFak and VNR-like integrins but displaying reduced adhesiveness to VN and EA.hy 926 endothelial cells. Our results suggest that C. albicans Fak-like protein is involved in the control of yeast cell adhesion to VN and endothelial cells.

scholarly journals Focal Adhesion Kinase Regulation of Mechanotransduction and its Impact on Endothelial Cell Functions

2012 ◽  
Vol 83 (1) ◽  
pp. 71-81 ◽  
Author(s):  
Noureddine Zebda ◽  
Oleksii Dubrovskyi ◽  
Konstantin G. Birukov
Keyword(s):  
Endothelial Cell ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Kinase Regulation ◽  
Cell Functions

scholarly journals Angiopoietin-1 Induces Endothelial Cell Sprouting Through the Activation of Focal Adhesion Kinase and Plasmin Secretion

2000 ◽  
Vol 86 (9) ◽  
pp. 952-959 ◽  
Author(s):  
Injune Kim ◽  
Hwan Gyu Kim ◽  
Sang-Ok Moon ◽  
Soo Wan Chae ◽  
June-No So ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Angiopoietin 1

scholarly journals Cordycepin Suppresses Endothelial Cell Proliferation, Migration, Angiogenesis, and Tumor Growth by Regulating Focal Adhesion Kinase and p53

Cancers ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 168 ◽  
Author(s):  
Yi-Ting Lin ◽  
Shu-Man Liang ◽  
Ya-Ju Wu ◽  
Yi-Ju Wu ◽  
Yi-Jhu Lu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Tumor Growth ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Epithelial Mesenchymal Transition ◽  
Endothelial Cell Proliferation ◽  
Mice Model ◽  
Mesenchymal Transition

Focal adhesion kinase (FAK) plays an important role in vascular development, including the regulation of endothelial cell (EC) adhesion, migration, proliferation, and survival. 3’-deoxyadenosine (cordycepin) is known to suppress FAK expression, cell migration, and the epithelial–mesenchymal transition in hepatocellular carcinoma (HCC). However, whether cordycepin affects FAK expression and cellular functions in ECs and the specific molecular mechanism remain unclear. In this study, we found that cordycepin suppressed FAK expression and the phosphorylation of FAK (p-FAK) at Tyr397 in ECs. Cordycepin inhibited the proliferation, wound healing, transwell migration, and tube formation of ECs. Confocal microscopy revealed that cordycepin significantly reduced FAK expression and decreased focal adhesion number of ECs. The suppressed expression of FAK was accompanied by induced p53 and p21 expression in ECs. Finally, we demonstrated that cordycepin suppressed angiogenesis in an in vivo angiogenesis assay and reduced HCC tumor growth in a xenograft nude mice model. Our study indicated that cordycepin could attenuate cell proliferation and migration and may result in the impairment of the angiogenesis process and tumor growth via downregulation of FAK and induction of p53 and p21 in ECs. Therefore, cordycepin may be used as a potential adjuvant for cancer therapy.

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