THC, CBD, CBN and CBG were found to inhibit human keratinocyte (skin cell) proliferation suggesting therapeutic potential in psoriasis (Wilkinson and Williamson, 2007).
The effect of THC is at least partially dependent on CB1. Given its affinity for CB receptors, CBN is also likely to function through CB1/2. CBD and CBG do not function through classical CB receptors and none of the phytocannabinoids depended on TRPV1 for their effect (in contrast to endocannabinoid function below), but PPARγ and GPR55 may be involved (Wilkinson and Williamson, 2007).
Similarly, the endocannabinoid Anandamide strongly suppresses keratinocyte proliferation and induces cell death via sequential activation of CB1 and TRPV1 (Tóth et al., 2011), suggesting the endocannabinoid system normally keeps keratinocyte proliferation in check.
Stimulating CB1 in human keratinocytes down-regulates keratins K6 and K16 which are involved in wound healing (Ramot et al., 2013), underlining the therapeutic relevance of the cannabinoid system in the treatment of psoriasis.
Ramot, Y., Sugawara, K., Zákány, N., Tóth, B.I., Bíró, T., and Paus, R. (2013). A novel control of human keratin expression: cannabinoid receptor 1-mediated signaling down-regulates the expression of keratins K6 and K16 in human keratinocytes in vitro and in situ. PeerJ 1, e40.
Tóth, B.I., Dobrosi, N., Dajnoki, A., Czifra, G., Oláh, A., Szöllosi, A.G., Juhász, I., Sugawara, K., Paus, R., and Bíró, T. (2011). endocannabinoids modulate human epidermal keratinocyte proliferation and survival via the sequential engagement of cannabinoid receptor-1 and transient receptor potential vanilloid-1. J. Invest. Dermatol. 131, 1095–1104.
Wilkinson, J.D., and Williamson, E.M. (2007). cannabinoids inhibit human keratinocyte proliferation through a non-CB1/CB2 mechanism and have a potential therapeutic value in the treatment of psoriasis. J. Dermatol. Sci. 45, 87–92.