GJICgap junctional intercellular communication
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In this study, we have investigated the role of Cx43 and GJIC in the rescue of CFTR-dependent chloride efflux in coculture of CFBE cells with hAMSCs.
Overall, in this study, we used six hAMSC isolates: three for analysis of Cx43 mRNA/protein expression and GJIC and another three for analysis of CFTR protein expression/function and paracellular permeability.
found that the proinflammatory cytokines IL-1[beta] and TNF-[alpha] reduced the intercellular communication via Cx43 GJIC, whereas it increased the cellular exchange with the extracellular milieu via Cx43 HCs [75].
TNF-a activated Cx43-HCs, rather than GJIC, to release CXCL1 [94], which could be blocked by Gap26, Gap27, and Cx43-siRNA in cultured astrocytes from the cortex and spinal cord of the SCI mouse model, a mouse model for chronic neuropathic pain (Table 1).
Influence of ELF-EMFs Treatments on C2C12 Myoblast cx43 Expression and GJIC. The effects of ELF-EMF treatments on differentiating C2C12 myoblasts were also evaluated by an analysis of the efficiency of their gap-junction coupling (dye-transfer efficiency) and by determining their expression levels of cx43, the major gap-junction component in skeletal myoblasts [20, 31, 32].
In addition, published data have strongly supported a key role for GJIC in the first phase of myogenic differentiation, when myoblasts that are committed to differentiate then adhere and fuse, to form gap junctions.
In the present study, the FRAP was used to determine the effect of the magnesium on GJIC in normal human osteoblasts.
Compared to the control group, the GJIC of osteoblasts was significantly promoted by the magnesium (P<0.05).
Here we found that hyperthermia induced JNK-dependent changes in Cx43 expression and GJIC in HeLa cells expressing exogenous Cx43-EGFP and in SkMs expressing endogenous Cx43.
The regulation of GJIC and connexin protein expression by steroids has been documented in several cell types (28-30), including ovarian cells (31); causing either a downregulation or an elevation in the expression of gap junctional proteins.
Other mechanisms including cell toxicity, mitogenesis, and inhibition of GJIC have been postulated (64-71).
The effects of the neuropeptides and HBMP2 on GJIC were determined by fluorescence recovery after photo-bleaching (FRAP) using a laser scanning confocal microscope.