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Activation of urothelial PAR1 receptors, either by locally generated thrombin or proteases present in the urine, may mediate bladder inflammation by inducing urothelial MIF release and upregulating urothelial MIF expression.
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Several reports have suggested that neuropeptide-containing, capsaicin-sensitive bladder afferents may mediate urinary bladder overactivity [ 27- 29].
Second, CXCR4 activation may mediate pain hypersensitivity in the bladder.
Alternatively, periplasmic proteases may mediate proteostasis of these amyloidogenic proteins.
EN2 secretion may mediate anti-viral changes in the stroma.
Some of these channels may mediate mechanosensory responses.
Some experts believe that they may mediate the effects of other cannabinoids.
Both moieties may mediate atherogenicity.
Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine expressed by urothelial cells that mediates bladder inflammation.
These results indicate that activation of PAR1 receptors mediates MIF release from urothelial cell which can then mediate MIF-mediated bladder inflammation, given MIF's pro-inflammatory role in the bladder [6].
As ICs are also found in the human bladder, it has been proposed that they mediate autonomous bladder activity [ 2].
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