It has been proposed that, under oxygen deprivation, Ca2+ is released from mitochondria into the cytosol (Subbaiah et al. 1994); the elevated cytosolic Ca2+ may provoke subsequent activation of kinases and phosphatases during aerenchyma formation (Subbaiah and Sachs 2003).
A major drawback of experimental models employing isolated liver macrophages is the digestion procedure required to detach macrophages from liver tissue, since this is associated with an enhanced generation of damage-associated molecular patterns (DAMP) originating from tissue disintegration, which may provoke DAMP-induced activation of respective macrophages (Chen and Nunez 2010).
Trigeminovascular activation may provoke release of multiple excitatory neurotransmitters including substance P, neurokinin A, and CGRP from dural afferent terminals, resulting in neurogenic vasodilation of dural blood vessels, release of proinflammatory mediators, degranulation of mast cells and plasma protein extravasation.
It has been hypothesized that the thrombotic-fibrinolytic imbalance after moderate or severe TBI may provoke an ischemic diathesis by the activation of hemostatic mechanisms and the inhibition of natural anticoagulation cascades [ 1, 2, 21, 22].
Injury of the mucous membranes cells may provoke the production of active oxygen species.
This phenomenon may provoke the pathways of mitogen-activated protein kinase (MAPK), phosphatidyl inositol-3-phosphate kinase (PI3K), and MAPK8 activation [ 12], which can modulate cell proliferation or death.
We were able to reproduce the ras-enhancing effect (Figure 7B), indicating that a strong activation of either pathway may provoke the enhancement of p53 transcription.
Up regulation of proapoptotic member of Bcl2 family (Bax) protein and apoptotic executor caspase-3 was noticed as indicated in Figure 8. Selim and Hendi [ 22] observed that activation of Bax protein may provoke permeabilisation of outer mitochondria membrane and resulted in the release of a soluble protein from intermembrane space into the cytosol, thereby promoting caspase activation.
Any type of neuronal injury may provoke the neuro-excitatory cascade, starting off with excessive calcium influx, glutamate receptor activation, neuronal hyperexcitability, eventually leading to cell death even after reperfusion and normalization of glutamate levels.
Classical explanations of how infectious agents may provoke autoimmunity [ 21] fit into the aforementioned conceptual framework at three levels: first, through the incorrect activation of the IIS – bystander activation; second, through a failure in IIS-AIS communication – epitope spreading; and third, through a non-specific adaptive response – molecular mimicry and superantigens.
