ACT1 redirects uncoupled Cx43 hemichannels into gap junctions, thereby reducing gap junction turnover and enhancing gap junction aggregation, without effecting Cx43 protein levels [ 33, 34].
The effect of enhancing gap junction function by 100 1000 nM rotigaptide (ZP123) and block by 30 μM carbenoxolone on these parameters was measured.
Carotenoids have been shown to suppress the in vitro cancer cell propagation by inducing differentiation and apoptosis, thus enhancing gap-junctional communication and inhibiting the cell cycle [ 49- 52].
Our data are compatible to the previous studies, indicating that 100 nM rotigaptide should be the best effective dose for enhancing gap junction conductance and preserving/ improving atrial conduction time.
This indicates that administration of dexamethasone enhanced GAP-43 expression levels.
Whether humans with rheumatoid arthritis show enhanced GAP-43 expression has not been explored, to our knowledge.
CaMKII has also been shown to mediate enhanced gap junctional coupling, mostly through Cx43, in response to high extracellular K+ in mouse spinal cord astrocytes [ 127].
Co-culturing also appears to enhance gap junctional intercellular communication as indicated by increased dye-coupled communication (Rojkind et al., 1995).
Adding to the complexity, Strohschein et al. (2011) showed that Aqp4 deletion enhances gap-junctional coupling, which would facilitate K+ redistribution through the astroglial syncytium.
Here, we first evaluated BT474 cells for ACT1 treatment-mediated effects on gap junction function by gap-FRAP and found that ACT1 treatment enhanced gap junction activity (Additional file 1: Figure S4A).
Despite no associations found between GAP-43 and frequency of seizures or interictal spikes in three groups of patients studied, it is possible that epileptic discharges may enhance GAP-43 expression.
