Activation of the canonical Wnt/β-catenin pathway enhances monocyte adhesion to endothelial cells
Biochemical and Biophysical Research Communications, ISSN: 0006-291X, Vol: 347, Issue: 1, Page: 109-116
2006
- 62Citations
- 36Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations62
- Citation Indexes62
- 62
- CrossRef52
- Captures36
- Readers36
- 36
Article Description
Monocyte adhesion to vascular endothelium has been reported to be one of the early processes in the development of atherosclerosis. In an attempt to develop strategies to prevent or delay atherosclerosis progression, we analyzed effects of the Wnt/β-catenin signaling pathway on monocyte adhesion to various human endothelial cells. Adhesion of fluorescein-labeled monocytes to various human endothelial cells was analyzed under a fluorescent microscope. Unlike sodium chloride, lithium chloride enhanced monocyte adhesion to endothelial cells in a dose-dependent manner. We further demonstrated that inhibitors for glycogen synthase kinase (GSK)-3β or proteosome enhanced monocyte-endothelial cell adhesion. Results of semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR) indicated that activation of Wnt/β-catenin pathway did not change expression levels of mRNA for adhesion molecules. In conclusion, the canonical Wnt/β-catenin pathway enhanced monocyte-endothelial cell adhesion without changing expression levels of adhesion molecules.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0006291X06013532; http://dx.doi.org/10.1016/j.bbrc.2006.06.082; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=33745758081&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/16815294; https://linkinghub.elsevier.com/retrieve/pii/S0006291X06013532; https://dx.doi.org/10.1016/j.bbrc.2006.06.082
Elsevier BV
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