Enzymes and Receptors of Prostaglandin Pathways with Arachidonic Acid-derived Versus Eicosapentaenoic Acid-derived Substrates and Products*♦
- M. Wada, C. DeLong, W. Smith
- Biology, Environmental ScienceJournal of Biological Chemistry
- 3 August 2007
In vitro specificities of prostanoid enzymes and receptors toward EPA-derived, 3-series versus AA- derived, 2-series prostanoids substrates and products are reported and biochemical data predict that increasing phospholipid EPA/AA ratios in cells would dampen prostanoidal signaling.
Plasma tissue plasminogen activator and plasminogen activator inhibitor-1 in hospitalized COVID-19 patients
- Y. Zuo, M. Warnock, D. Lawrence
- Medicine, BiologyScientific Reports
- 15 January 2021
Data indicate that fibrinolytic homeostasis in COVID-19 is complex with a subset of patients expressing a balance of factors that may favor fibralelysis, and extremely high levels of tPA enhance spontaneous fibrinelysis and are significantly associated with mortality in some patients.
Alteration of cartilage metabolism by cells from osteoarthritic bone.
- C. Westacott, G. Webb, M. Warnock, J. Sims, C. Elson
- Biology, MedicineArthritis & Rheumatism
- 1 July 1997
Bone cells from OA patients can influence cartilage metabolism, which might explain why increased subchondral bone activity can predict cartilage loss.
Visceral Adipose Tissue Inflammation Accelerates Atherosclerosis in Apolipoprotein E-Deficient Mice
- M. Öhman, Yue-chun Shen, D. Eitzman
- Biology, MedicineCirculation
- 12 February 2008
The results indicate that visceral adipose-related inflammation accelerates atherosclerosis in mice and drugs such as thiazolidinediones might be a useful strategy to specifically attenuate the vascular disease induced by visceral inflammatory fat.
Mechanism of Inactivation of Plasminogen Activator Inhibitor-1 by a Small Molecule Inhibitor*
- N. Gorlatova, J. Cale, D. Lawrence
- Biology, ChemistryJournal of Biological Chemistry
- 23 March 2007
It is suggested for the first time a novel pool of PAI-1 exists that is vulnerable to inhibition by inactivators that bind at the vitronectin binding site.
Characterization of a Novel Class of Polyphenolic Inhibitors of Plasminogen Activator Inhibitor-1*
- J. Cale, Shih-Hon Li, D. Lawrence
- Biology, ChemistryJournal of Biological Chemistry
- 8 January 2010
A novel family of high affinity PAI-1-inactivating compounds with improved characteristics and in vivo efficacy is described, and it is suggested that the known cardiovascular benefits of dietary polyphenols may derive in part from their inactivation of PAi-1.
Plasma tissue plasminogen activator and plasminogen activator inhibitor-1 in hospitalized COVID-19 patients
- Y. Zuo, M. Warnock, D. Lawrence
- Medicine, BiologymedRxiv
- 2 September 2020
The data indicate that fibrinolytic homeostasis in COVID-19 is complex with a subset of patients expressing a balance of factors that may favor fibralelysis and suggests that further study of tPA as a potential biomarker is warranted.
Imatinib treatment reduces brain injury in a murine model of traumatic brain injury
- E. Su, L. Fredriksson, D. Lawrence
- BiologyFrontiers in Cellular Neuroscience
- 7 October 2015
It is shown that Imatinib treatment, begun 45 min after TBI and given twice daily for 5 days, significantly reduces BBB dysfunction and this suggests a novel strategy for the treatment of TBI with an existing FDA approved antagonist of the PDGFRα.
Mechanisms of Arg-Pro-Pro-Gly-Phe inhibition of thrombin.
- A. Hasan, M. Warnock, A. Schmaier
- Biology, ChemistryAmerican Journal of Physiology. Heart and…
- 1 July 2003
RPPGF binds to PAR1 to prevent thrombin cleavage at Arg41 and interacts with the active site of alpha-thrombin, indicating that RPPGF is a bifunctional inhibitor of thrombocytin.
Angiotensin 1-7 and Mas decrease thrombosis in Bdkrb2-/- mice by increasing NO and prostacyclin to reduce platelet spreading and glycoprotein VI activation.
- Chao Fang, E. Stavrou, A. Schmaier
- Biology, MedicineBlood
- 11 April 2013
Bdkrb2(-/-) platelets have reduced collagen-related peptide-induced integrin α2bβ3 activation and P-selectin expression that are partially corrected by in vivo A-779, nimesulide, or L-NAME treatment.
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