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The role of carotenoids and retinoids in gap junctional communication
1Institut für Physiologische Chemie I, Heinrich-Heine-Universität Düsseldorf, Germany.
Abstract:
Induction of gap junctional communication (GJC) is discussed as one possible mechanism underlying the cancer-preventive properties of carotenoids. Structurally different carotenoids have different effects on this GJC pathway. Beta-carotene, echinenone, canthaxanthin, cryptoxanthin and 4-hydroxy-beta-carotene efficiently induce GJC in murine fibroblasts. Decomposition products of canthaxanthin (e.g. 4-oxo-retinoic acid) enhance both GJC and expression of connexin 43 mRNA. Thus, the biological activity of canthaxanthin is due at least in part to formation of active decomposition products such as 4-oxo-retinoic acid. A number of other small molecules such as 1,25-dihydroxycholecalciferol or thyroid hormones serve as nuclear receptor ligands. Cholecalciferol, 3,3',5-triiodo-L-thyronine and L-thyroxine induce GJC to a similar extent as carotenoids or retinoic acid. Interactions between these signalling pathways may be involved in GJC regulation.
Insights
Carotenoids and certain other molecules like vitamin D can boost cancer prevention by enhancing gap junctional communication (GJC). Some carotenoid breakdown products are key to this effect, highlighting complex molecular interactions.
Area of Science:
- Molecular Biology
- Cell Biology
- Cancer Research
Background:
- Gap junctional communication (GJC) is a crucial cellular process potentially involved in cancer prevention.
- Carotenoids are known for their potential health benefits, including cancer prevention, with GJC induction being a proposed mechanism.
- The specific effects of different carotenoids and their metabolites on GJC are not fully elucidated.
Purpose of the Study:
- To investigate the role of various carotenoids and related compounds in inducing GJC.
- To explore the contribution of carotenoid decomposition products to GJC modulation.
- To examine the potential involvement of nuclear receptor ligands, such as vitamin D and thyroid hormones, in GJC regulation.
Main Methods:
- Assays to measure GJC induction in murine fibroblast models.
- Analysis of connexin 43 mRNA expression following treatment with carotenoids and their derivatives.
- Comparison of GJC-inducing effects of carotenoids with those of known nuclear receptor ligands.
Main Results:
- Several carotenoids (beta-carotene, echinenone, canthaxanthin, cryptoxanthin, 4-hydroxy-beta-carotene) efficiently induced GJC.
- Decomposition products of canthaxanthin, such as 4-oxo-retinoic acid, were found to enhance both GJC and connexin 43 mRNA expression.
- Other small molecules, including cholecalciferol and thyroid hormones (3,3',5-triiodo-L-thyronine, L-thyroxine), also induced GJC, comparable to carotenoids and retinoic acid.
Conclusions:
- Carotenoids, and particularly their active decomposition products like 4-oxo-retinoic acid, play a significant role in inducing GJC, which may underlie their cancer-preventive effects.
- The induction of GJC by various compounds, including carotenoids, vitamin D metabolites, and thyroid hormones, suggests complex signaling pathway interactions in cellular communication and potentially cancer chemoprevention.