Phosphovimentin appeared as one of the proteins associated with biotinylated plasma membrane-bound proteins in 5HT-stimulated platelets.
SERT could be one of the other phosphovimentin-associated membrane proteins, but our co-IP data in 5HT-stimulated platelets also demonstrated an elevation in the association of SERT-phosphovimentin in whole platelet ().
The level of phosphovimentin on the plasma membrane 5HT-stimulated platelet was evaluated.
The highest amount of SERT was pulled down by vimentin-Ab in 2 nM 5HT-stimulated platelets.
If platelets aggregate at atherosclerotic lesions and release serotonin, and vasoconstrictor responses to serotonin are greatly potentiated in atherosclerotic arteries, serotonin may be an important mediator of vasospasm.
Upregulation of these two stress parameters is atherogenic: epinephrine-activated platelets stimulating thrombin formation interact with endothelial cells activated by angiotensin II to cause, first, smooth muscle cell proliferation, which is a histological hallmark of atherosclerosis, and, lastly, a symptomatic thrombotic occlusion-the stroke.
Finally, platelets and platelet-derived serotonin aggravate viral hepatitis by affecting the microcirculation in the liver.
On one hand, platelets bind to the activated sinusoidal endothelium and induce apoptosis of these cells; on the other hand, platelet-derived serotonin assists in repair of the ischemic tissue.
Serotonin effects on platelets are not only mediated by receptor binding but also by covalently binding effector proteins (serotonylation) in the platelet cytoplasm and on the platelet surface.
The paper under evaluation here introduces the concept that platelet-derived serotonin supports virus persistence in the liver and aggravates CTL-mediated liver immunopathology.
5-HT, monoamine oxidase (MAO-B) activities and amounts were measured in platelets, and 5-hydroxyindolacetic acid (5-HIAA)—the 5-HT/MAO catabolite—in plasma samples.
The untransformed 5-HT released from platelet into plasma is largely diluted, and plasma 5-HT concentrations were not significantly different between the three groups (not shown).
Under normal physiological conditions, however, platelet granule-stored 5-HT can be either released into the blood flow through the open canalicular system or exposed to the platelet mitochondrial monoamine oxidase (MAO).
Moreover, platelet5-HT and plasma 5-HIAA levels were highly correlated (P<0.001, not shown) with both platelet MAO activities and protein concentration.
Once synthesized in the gastrointestinal tract, peripheral 5-HT is actively taken up by platelets which store the amine within their dense granules.
Acutely, the physiologic function of serotonin released from mast cells or platelets could be to locally increase ciliary beat frequency.
Since arterioles, capillaries, and venules are found immediately underneath the airway epithelium, serotonin released from platelets could also reach the airway epithelium especially when postcapillary venules and capillaries become leaky during inflammation and thereby increase cilia-driven particle transport.
Another ubiquitous source of serotonin that is shared by rodents and humans are platelets.
These results indicate that serotonin is a likely endogenous mediator that can increase cilia-driven transport independent from acetylcholine during activation of mast cells and platelets.
Whether norepinephrine should be avoided in the second post-traumatic week and whether norepinephrine-stimulated platelets might induce additional brain damage warrant further investigations.
• In vitro stimulation of isolated platelets unmasks functional changes. • Norepinephrine, in a concentration-dependent manner, stimulates isolated platelets in healthy volunteers and critically ill patients with severe traumatic brain injury. • Stimulation was similar in arterial and jugular venous platelets. • Isolated platelets express a temporally heterogeneous susceptibility to norepinephrine-mediated stimulation, reflected by a decreased response during the first week followed by an increased stimulation in the second week. • In the second week, increased platelet susceptibility to norepinephrine-mediated stimulation coincided with signs of cerebral worsening.
Norepinephrine-mediated activation of platelets
During the second week, norepinephrine-mediated increase in P-selectin-positive and microparticle-positive platelets significantly exceeded the changes observed during the first week and the corresponding alterations found in volunteers.
During the first week following TBI, norepinephrine-mediated stimulation of isolated platelets was significantly reduced compared with volunteers (control).
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