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The Effect of Naphthoquinones on Gap Junctional Intercellular Communication Open Access


Other title
Intercellular Communication
Gap Junction
Type of item
Degree grantor
University of Alberta
Author or creator
AL Omair, Omar Abdulrahman
Supervisor and department
Klotz, Lars-Oliver (Faculty of Pharmacy & Pharmaceutical Sciences)
Examining committee member and department
Siraki, Arno (Pharmacy and Pharmaceutical Sciences)
Persad, Sujata (Department of Pediatrics)
Marsh, Sharon (Pharmacy and Pharmaceutical Sciences)
Faculty of Pharmacy and Pharmaceutical Sciences
Pharmaceutical Sciences
Date accepted
Graduation date
Master of Science
Degree level
Gap junctions are groups of channels that connect two neighboring cells, allowing for the passage of small molecules, such as nutrients and signalling factors, between cytosols. Gap junctional channels consist of building blocks called connexins. Cancer cells exhibit a low basal level of gap junctional intercellular communication (GJIC), and experimental animals that lack certain connexins were shown to develop cancer at faster rates than their healthy counterparts. Here, we investigate the effect of synthetic and natural naphthoquiones on connexin43 and on GJIC in order to identify potential modes of interference of quinoid compounds with cellular pathways that control GJIC. WB-F344 rat liver epithelial cells were exposed to synthetic and natural naphthoquinones. Phosphorylation of connexin-43, the epidermal growth factor receptor (EGFR) and extracellular signal-regulated kinases (ERK-1, -2), were analysed by Western blotting. Naphthoquinone toxicity profiles were established using neutral red uptake for assessment of cell viability. Assessment of GJIC was performed by microinjection of a channel-permeant fluorescent dye, Lucifer yellow, into single cells and microscopic analysis of its spreading to cells adjacent to injected cells. Of the naphthoquinones tested, menadione (2-methyl-1,4-naphthoquinone, MQ), 2-methoxy-1,4-naphthoquinone (MNQ) and 2,3-dimethoxy-1,4-naphthoquinone (DMNQ) caused a significant phosphorylation of connexin-43 at different concentrations. In line with this, GJIC was significantly downregulated after 20 min of exposure to MQ, MNQ or DMNQ. In conclusion, Redox-cycling naphthoquinones (with exclusive redox-cyclers, such as DMNQ, and alkylating/redox-cycling naphthoquinones, such as MQ and MNQ) stimulate connexin phosphorylation and a loss of GJIC.
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