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HighlightsFunctional cannabinoid CB2 receptors are upregulated upon injury in corneal epithelium. CB2 receptor deletion impairs the course of wound healing. CB2 receptors mediate chemorepulsion in corneal epithelial cells. CB2 receptors do not alter the epithelial cell proliferation. Findings suggest that like CB1, cannabinoid CB2 receptors play a role in the course of wound healing, but via chemorepulsion.
Thus, the cannabinoid-cannabinoid receptor system may prove therapeutically manageable in ablating neuropathogenic disorders such as Alzheimer’s disease, multiple sclerosis, amyotrophic lateral sclerosis, HIV encephalitis, closed head injury, and granulomatous amebic encephalitis.
This increased availability of endocannabinoids might stimulate cannabinoid receptors in a pathophysiological manner.
Our results indicate that definite activation of the cannabinoid receptors exerted different effects in atMSCs, which could be of specific value in cell-based therapy for wound regeneration.
However, emerging evidences suggest the role of cannabinoid receptors (CBRs) in curtailing the progression of PD by activating neuroprotective pathways.
Moreover, in primary cultured neurons, the low endocytotic agonist Δ9‐THC or anandamide exhibited a greater desensitization of endogenous CB1 receptors than the high endocytotic agonist WIN 55,212‐2, CP 55940 or 2‐arachidonoyl glycerol, indicating that cannabinoids with high endocytotic efficacy might cause reduced development of cannabinoid tolerance to some kind cannabinoid‐mediated effects.
In addition to identifying a potential drug treatment for painful neuropathy, this study suggests that changes in cannabinoid receptors occurs in nerve injured animals.
In diseases for which cannabinoid receptors are protective, knowledge of the mechanisms of receptor up-regulation could be used to design therapies to regionally increase receptor expression and thus increase efficacy of an agonist.
In particular, emerging evidence suggests that agonists of cannabinoid receptors expressed by tumor cells may offer a novel strategy to treat cancer.
Moreover, region-specific adaptations in CB1 receptors following chronic cannabinoid administration may produce differential adaptations at the in vivo level.
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