Stability of von Willebrand Factor secretion in different human endothelial hybrid cell lines

1992 ◽  
Vol 8 (1) ◽  
pp. 31-37 ◽  
Author(s):  
O. Hohenwarter ◽  
C. Schmatz ◽  
H. Katinger
Keyword(s):  
Cell Lines ◽  
Von Willebrand Factor ◽  
Hybrid Cell ◽  
Von Willebrand ◽  
Hybrid Cell Lines ◽  
Willebrand Factor ◽  
Factor Secretion

scholarly journals A method for identification of vocal fold lamina propria fibroblasts in culture

2008 ◽  
Vol 139 (6) ◽  
pp. 816-822 ◽  
Author(s):  
Susan L. Thibeault ◽  
Wenhua Li ◽  
Stephanie Bartley
Keyword(s):  
Lamina Propria ◽  
Cell Lines ◽  
Von Willebrand Factor ◽  
Vocal Fold ◽  
Fibroblast Cell ◽  
Cytokeratin 19 ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Area Of Study

Objective Vocal fold biology research is emerging as a vital area of study in laryngology. One impediment is the lack of both commercially available vocal fold lamina propria fibroblasts and a constitutively expressed specific marker for fibroblasts. We present an in vitro technique that allows for identification of fibroblasts by ruling out the possibility of the cells belonging to other lineages that are found in vocal fold tissue. Study Design An in vitro study. Methods Two primary vocal fold fibroblast cell lines and one immortalized vocal fold fibroblast cell line were cultured. Immunohistologic staining for α-actinin, cytokeratin 19, and von Willebrand factor was completed for the three fibroblast lines in addition to skeletal, endothelial, and epithelial cell lines. Cell type was differentiated by positive staining for α-actinin, cytokeratin 19, and von Willebrand factor. Results Fibroblast cultures did not express α-actinin, cytokeratin 19, and von Willebrand factor, whereas skeletal muscle, endothelial, and epithelial cultured cells expressed each respectively. Conclusions This simple rule-out methodology for fibroblast confirmation is an important step when establishing cell culture, and it establishes sound internal validity particularly in the early stages of this emerging area of study.

Multi-Cellular Activation In Vivo by Endotoxin in Humans – Limited Protection by Adenosine Infusion

2000 ◽  
Vol 84 (09) ◽  
pp. 381-387 ◽  
Author(s):  
Nailin Li ◽  
Anne Soop ◽  
Alf Sollevi ◽  
Paul Hjemdahl
Keyword(s):  
Von Willebrand Factor ◽  
Thrombin Generation ◽  
Platelet Reactivity ◽  
Adenosine Infusion ◽  
Cellular Activation ◽  
Soluble P ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Factor Secretion

SummaryThe influence of adenosine infusion (40 µg/kg/min for 4 h) on inflammatory and hemostatic parameters was investigated in healthy males without (n = 10) or with (n = 11) intravenous endotoxin injection (4 ng/kg). Without endotoxin, adenosine elevated circulating leukocytes and circulating platelet-leukocyte aggregates. Endotoxin activated platelets and leukocytes in vivo. Platelet activation was seen as slightly increased platelet P-selectin expression, decreased platelet counts, and elevated plasma soluble P-selectin (from 39.6 ± 3.4 to 68.9 ± 6.6 ng/ml; P <0.01). Leukocyte activation was evidenced by increased CD11b expression (from MFI of 0.54 ± 0.02 to 2.21 ± 0.17; P <0.01) and plasma elastase levels (from 25.3 ± 2.5 to 169.3 ± 22.5 ng/ml; P <0.01). Endotoxin also enhanced platelet and leukocyte responsiveness to in vitro stimulation. Endotoxin induced von Willebrand factor secretion (from 92 ± 8 units to 265 ± 19 units at 4 h; P <0.001) and enhanced thrombin generation in vivo. Endotoxin induced leukocytosis and thus increased circulating platelet-leukocyte, mainly platelet-neutrophil, aggregates. Adenosine caused slight attenuation of platelet reactivity to agonist stimulation, enhanced the endotoxin-induced leukocytosis, and detained more platelet-leukocyte aggregates in circulation, but did not attenuate endotoxin-induced neutrophil elastase secretion, von Willebrand factor secretion, or thrombin generation. Thus, endotoxemia induces multi-cellular activation in vivo. Adenosine inhibits leukocyte adhesion and extravasation, and mildly attenuates platelet responsiveness and soluble P-selectin release. Adenosine has the potential of becoming a therapeutic antiinflammatory drug, but an optimal treatment strategy needs to be developed.

scholarly journals Weibel-Palade Body Localized Syntaxin-3 Modulates Von Willebrand Factor Secretion From Endothelial Cells

2018 ◽  
Vol 38 (7) ◽  
pp. 1549-1561 ◽  
Author(s):  
Maaike Schillemans ◽  
Ellie Karampini ◽  
Bart L. van den Eshof ◽  
Anastasia Gangaev ◽  
Menno Hofman ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Von Willebrand Factor ◽  
Syntaxin 3 ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Factor Secretion

The NFY Transcription Factor Mediates Induction of the von Willebrand Factor Promoter by Irradiation

2001 ◽  
Vol 85 (05) ◽  
pp. 837-844 ◽  
Author(s):  
Angela Bertagna ◽  
Nadia Jahroudi
Keyword(s):  
Transcription Factor ◽  
Von Willebrand Factor ◽  
Thrombus Formation ◽  
Core Promoter ◽  
Transcriptional Level ◽  
Cis Acting ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Factor Secretion

SummaryIonizing irradiation in patients is proposed to cause thrombus formation. An increase in von Willebrand factor secretion in response to irradiation is a major contributing factor to thrombus formation. We have previously reported that the increased VWF secretion in response to irradiation is mediated at the transcriptional level. The VWF core promoter fragment (sequences –90 to +22) was shown to contain the necessary cis-acting element(s) to mediate the irradiation response of the VWF gene. Here we report that a CCAAT element in the VWF promoter is the cis-acting element necessary for irradiation induction and that the NFY transcription factor interacts with this element. These analyses demonstrate that inhibition of NFY’s interaction with the CCAAT element abolishes the irradiation induction of the VWF promoter. These results provide a novel role for NFY and add this factor to the small list of irradiation-responsive transcription factors. Coimmunoprecipitation experiments demonstrated that NFY is associated with the histone acetylase P/CAF in vivo and that irradiation resulted in an increased association of NFY with coactivator P/CAF. We propose that irradiation induction of the VWF promoter involves a mechanism resulting in increased recruitment of the coactivator P/CAF to the promoter via the NFY transcription factor.

scholarly journals Dopamine modulates von Willebrand factor secretion in endothelial cells via D2-D4 receptors

2006 ◽  
Vol 4 (7) ◽  
pp. 1588-1595 ◽  
Author(s):  
S. ZAREI ◽  
M. FRIEDEN ◽  
B. RUBI ◽  
P. VILLEMIN ◽  
B. R. GAUTHIER ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Von Willebrand Factor ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Factor Secretion

cAMP-induced secretion of endothelial von Willebrand factor is regulated by a phosphorylation/dephosphorylation switch in annexin A2

Blood ◽  
2013 ◽  
Vol 122 (6) ◽  
pp. 1042-1051 ◽  
Author(s):  
Ines Brandherm ◽  
Jennifer Disse ◽  
Dagmar Zeuschner ◽  
Volker Gerke
Keyword(s):  
Complex Formation ◽  
Von Willebrand Factor ◽  
Annexin A2 ◽  
Key Points ◽  
Von Willebrand ◽  
Willebrand Factor ◽  
Factor Secretion

Key Points A calcineurin-like phosphatase dephosphorylates annexin A2 in the course of cAMP-induced Weibel-Palade body exocytosis. Dephosphorylation at serine 11 of annexin A2 triggers complex formation with S100A10 that is required for von Willebrand factor secretion.

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