scholarly journals Serum amyloid A mediates the inhibitory effect of Ganoderma lucidum polysaccharides on tumor cell adhesion to endothelial cells

1994 ◽  
Author(s):  
Ying-Bo
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Tumor Cell ◽  
Ganoderma Lucidum ◽  
Serum Amyloid A ◽  
Inhibitory Effect ◽  
Serum Amyloid ◽  
Tumor Cell Adhesion ◽  
Amyloid A ◽  
Ganoderma Lucidum Polysaccharides

scholarly journals The vacuolar-type ATPase inhibitor archazolid increases tumor cell adhesion to endothelial cells by accumulating extracellular collagen

PLoS ONE ◽  
2018 ◽  
Vol 13 (9) ◽  
pp. e0203053 ◽  
Author(s):  
Betty Luong ◽  
Rebecca Schwenk ◽  
Jacqueline Bräutigam ◽  
Rolf Müller ◽  
Dirk Menche ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Tumor Cell ◽  
Atpase Inhibitor ◽  
Tumor Cell Adhesion

Serum amyloid A activation of human coronary artery endothelial cells exhibits a neutrophil promoting molecular profile

2013 ◽  
Vol 90 ◽  
pp. 55-63 ◽  
Author(s):  
Katja Lakota ◽  
Katjusa Mrak-Poljsak ◽  
Borut Bozic ◽  
Matija Tomsic ◽  
Snezna Sodin-Semrl
Keyword(s):  
Endothelial Cells ◽  
Coronary Artery ◽  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Molecular Profile ◽  
Human Coronary Artery ◽  
Amyloid A

scholarly journals Serum amyloid A induces endothelial dysfunction in porcine coronary arteries and human coronary artery endothelial cells

2008 ◽  
Vol 295 (6) ◽  
pp. H2399-H2408 ◽  
Author(s):  
Xinwen Wang ◽  
Hong Chai ◽  
Zehao Wang ◽  
Peter H. Lin ◽  
Qizhi Yao ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Coronary Artery ◽  
Endothelial Dysfunction ◽  
Coronary Arteries ◽  
Molecular Mechanisms ◽  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Dependent Manner ◽  
Amyloid A ◽  
Enos Mrna

The objective of this study was to determine the effects and mechanisms of serum amyloid A (SAA) on coronary endothelial function. Porcine coronary arteries and human coronary arterial endothelial cells (HCAECs) were treated with SAA (0, 1, 10, or 25 μg/ml). Vasomotor reactivity was studied using a myograph tension system. SAA significantly reduced endothelium-dependent vasorelaxation of porcine coronary arteries in response to bradykinin in a concentration-dependent manner. SAA significantly decreased endothelial nitric oxide (NO) synthase (eNOS) mRNA and protein levels as well as NO bioavailability, whereas it increased ROS in both artery rings and HCAECs. In addition, the activities of internal antioxidant enzymes catalase and SOD were decreased in SAA-treated HCAECs. Bio-plex immunoassay analysis showed the activation of JNK, ERK2, and IκB-α after SAA treatment. Consequently, the antioxidants seleno-l-methionine and Mn(III) tetrakis-(4-benzoic acid)porphyrin and specific inhibitors for JNK and ERK1/2 effectively blocked the SAA-induced eNOS mRNA decrease and SAA-induced decrease in endothelium-dependent vasorelaxation in porcine coronary arteries. Thus, SAA at clinically relevant concentrations causes endothelial dysfunction in both porcine coronary arteries and HCAECs through molecular mechanisms involving eNOS downregulation, oxidative stress, and activation of JNK and ERK1/2 as well as NF-κB. These findings suggest that SAA may contribute to the progress of coronary artery disease.

Binding of 13-HODE and 5-, 12- and 15-HETE to endothelial cells and subsequent platelet, neutrophil and tumor cell adhesion

1988 ◽  
Vol 961 (2) ◽  
pp. 153-159 ◽  
Author(s):  
Thomas A. Haas ◽  
Eva Bastida ◽  
Kumi Nakamura ◽  
Francoise Hullin ◽  
Lourdes Admirall ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Tumor Cell ◽  
Tumor Cell Adhesion

High Glucose Levels Enhance the Proinflammatory and Prothrombotic Actions of Serum Amyloid A (SAA) in Endothelial Cells

2010 ◽  
Vol 19 ◽  
pp. S58
Author(s):  
C. Song ◽  
K. Hsu ◽  
P. Witting ◽  
C. Geczy ◽  
S. Freedman
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Glucose Levels ◽  
Amyloid A

scholarly journals Colocalization of Serum Amyloid A with Microtubules in Human Coronary Artery Endothelial Cells

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Katja Lakota ◽  
Nataša Resnik ◽  
Katjuša Mrak-Poljšak ◽  
Snežna Sodin-Šemrl ◽  
Peter Veranič
Keyword(s):  
Endothelial Cells ◽  
Coronary Artery ◽  
Actin Filaments ◽  
Serum Amyloid A ◽  
Serum Amyloid ◽  
Mrna Levels ◽  
Human Coronary Artery ◽  
Double Labeling ◽  
Amyloid A ◽  
Cytoskeletal Elements

Serum amyloid A (SAA) acts as a major acute phase protein and represents a sensitive and accurate marker of inflammation. Besides its hepatic origin, as the main source of serum SAA, this protein is also produced extrahepatically. The mRNA levels of SAA become significantly elevated following proinflammatory stimuli, as well as, are induced through their own positive feedback in human primary coronary artery endothelial cells. However, the intracellular functions of SAA are so far unknown. Colocalization of SAA with cytoskeletal filaments has previously been proposed, so we analyzed the colocalization of SAA with all three cytoskeletal elements: actin filaments, vimentin filaments, and microtubules. Immunofluorescent double-labeling analyses confirmed by PLA method revealed a strict colocalization of SAA with microtubules and a very infrequent attachment to vimentin while the distribution of actin filaments appeared clearly separated from SAA staining. Also, no significant colocalization was found between SAA and endomembranes labeled with the fluorescent lipid stain DiO6. However, SAA appears to be located also unbound in the cytosol, as well as inside the nucleus and within nanotubes extending from the cells or bridging neighboring cells. These different locations of SAA in endothelial cells strongly indicate multiple potential functions of this protein.

Involvement of Nitric Oxide in Tumor Cell Adhesion to Cytokine-Activated Endothelial Cells

1992 ◽  
Vol 20 ◽  
pp. S155-S159 ◽  
Author(s):  
Maria J. Vidal ◽  
Mara R. Zocchi ◽  
Alessandro Poggi ◽  
Fabio Pellegatta ◽  
Sergio L. Chierchia
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Cell Adhesion ◽  
Tumor Cell ◽  
Tumor Cell Adhesion

scholarly journals Analysis of Differentially Expressed Genes in Endothelial Cells Following Tumor Cell Adhesion, and the Role of PRKAA2 and miR-124-3p

2021 ◽  
Vol 9 ◽  
Author(s):  
Yan Pan ◽  
Marhaba Abdureyim ◽  
Qing Yao ◽  
Xuejun Li
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Differentially Expressed Genes ◽  
Differentially Expressed ◽  
Expression Level ◽  
Luciferase Reporter ◽  
Tumor Cell Adhesion ◽  
Tumor Endothelium

Tumor cell adhesion to the endothelium is one pattern of tumor–endothelium interaction and a key step during tumor metastasis. Endothelium integrity is an important barrier to prevent tumor invasion and metastasis. Changes in endothelial cells (ECs) due to tumor cell adhesion provide important signaling mechanisms for the angiogenesis and metastasis of tumor cells. However, the changes happened in endothelial cells when tumor–endothelium interactions are still unclear. In this study, we used Affymetrix Gene Chip Human Transcriptome Array 2.0. and quantitative real-time PCR (qPCR) to clarify the detailed gene alteration in endothelial cells adhered by prostate tumor cells PC-3M. A total of 504 differentially expressed mRNAs and 444 lncRNAs were obtained through chip data analysis. Gene Ontology (GO) function analysis showed that differentially expressed genes (DEGs) mainly mediated gland development and DNA replication at the biological level; at the cell component level, they were mainly involved in the mitochondrial inner membrane; and at the molecular function level, DEGs were mainly enriched in ATPase activity and catalytic activity. Kyoto Encyclopedia of Genes and Genomes (KEGG) signal pathway analysis showed that the DEGs mainly regulated pathways in cancer, cell cycle, pyrimidine metabolism, and the mTOR signaling pathway. Then, we constructed a protein–protein interaction functional network and mRNA–lncRNA interaction network using Cytoscape v3.7.2. to identify core genes, mRNAs, and lncRNAs. The miRNAs targeted by the core mRNA PRKAA2 were predicted using databases (miRDB, RNA22, and Targetscan). The qPCR results showed that miR-124-3p, the predicted target miRNA of PRKAA2, was significantly downregulated in endothelial cells adhered by PC-3M. With a dual luciferase reporter assay, the binding of miR-124-3p with PRKAA2 3’UTR was confirmed. Additionally, by using the knockdown lentiviral vectors of miR-124-3p to downregulate the miR-124-3p expression level in endothelial cells, we found that the expression level of PRKAA2 increased accordingly. Taken together, the adhesion of tumor cells had a significant effect on mRNAs and lncRNAs in the endothelial cells, in which PRKAA2 is a notable changed molecule and miR-124-3p could regulate its expression and function in endothelial cells.

scholarly journals NFkB Inhibition Mitigates Serum Amyloid A-Induced Pro-Atherogenic Responses in Endothelial Cells and Leukocyte Adhesion and Adverse Changes to Endothelium Function in Isolated Aorta

2018 ◽  
Author(s):  
Abigail Vallejo ◽  
Belal Chami ◽  
Joanne M. Dennis ◽  
Martin Simone ◽  
Gulfam Ahmad ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Vascular Function ◽  
Serum Amyloid A ◽  
Ex Vivo ◽  
Early Stage ◽  
Leukocyte Adhesion ◽  
Serum Amyloid ◽  
Amyloid A ◽  
Isolated Aorta

The acute phase protein serum amyloid A (SAA) is associated with endothelial dysfunction and early-stage atherogenesis. Stimulation of vascular cells with SAA increases gene expression of pro-inflammation cytokines and tissue factor (TF). Activation of the transcription factor, nuclear factor kappa-B (NFkB), may be central to SAA-mediated endothelial cell inflammation, dysfunction and pro-thrombotic responses, while targeting NFkB with a pharmacologic inhibitor, BAY11-7082, may mitigate SAA activity. Human carotid artery endothelial cells (HCtAEC) were pre-incubated (1.5 h) with 10 µM BAY11-7082 or vehicle (control) followed by SAA (10 μg/mL; 4.5 h). Under these conditions gene expression for TF and TNF increased in SAA-treated HCtAEC and pre-treatment with BAY11-7082 significantly (TNF) and marginally (TF) reduced mRNA expression. Intracellular TNF and IL-6 protein also increased in HCtAEC supplemented with SAA and this expression was inhibited by BAY11-7082. Supplemented BAY11-7082 also significantly decreased SAA-mediated leukocyte adhesion to apolipoprotein E-deficient mouse aorta in ex vivo vascular flow studies. In vascular function studies, isolated aortic rings pre-treated with BAY11-7082 prior to incubation with SAA showed improved endothelium-dependent vasorelaxation and increased vascular cGMP content. Together these data suggest that inhibition of NFkB activation may protect endothelial function by inhibiting the pro-inflammatory and pro-thrombotic activities of SAA.

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