Abstract | BACKGROUND: METHODS AND RESULTS: CONCLUSIONS: These data demonstrate a nontranscriptional activity of STAT3 that facilitates a crosstalk between proinflammatory cytokine and hemostasis/ thrombosis signals in platelets. This crosstalk may be responsible for the platelet hyperactivity found in conditions of inflammation.
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Authors | Zhou Zhou, Francisca C Gushiken, Doug Bolgiano, Breia J Salsbery, Niloufar Aghakasiri, Naijie Jing, Xiaoping Wu, K Vinod Vijayan, Rolando E Rumbaut, Roberto Adachi, Jose A Lopez, Jing-Fei Dong |
Journal | Circulation
(Circulation)
Vol. 127
Issue 4
Pg. 476-485
(Jan 29 2013)
ISSN: 1524-4539 [Electronic] United States |
PMID | 23266857
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, U.S. Gov't, Non-P.H.S.)
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Chemical References |
- IL6 protein, human
- Interleukin-6
- Intracellular Signaling Peptides and Proteins
- STAT3 Transcription Factor
- STAT3 protein, human
- Stat3 protein, mouse
- Collagen
- Protein-Tyrosine Kinases
- SYK protein, human
- Syk Kinase
- Syk protein, mouse
- Phospholipase C gamma
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Topics |
- Animals
- Atherosclerosis
(metabolism)
- Blood Platelets
(cytology, drug effects, metabolism)
- Collagen
(metabolism, pharmacology)
- HEK293 Cells
- Humans
- Interleukin-6
(metabolism)
- Intracellular Signaling Peptides and Proteins
(antagonists & inhibitors, metabolism)
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Phospholipase C gamma
(metabolism)
- Phosphorylation
(physiology)
- Platelet Aggregation
(physiology)
- Protein-Tyrosine Kinases
(antagonists & inhibitors, metabolism)
- STAT3 Transcription Factor
(genetics, metabolism)
- Signal Transduction
(physiology)
- Syk Kinase
- Thrombosis
(metabolism)
- Vasculitis
(metabolism)
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