Background: Psoriasis is a chronic recurrent inflammatory disease. Mesenchymal stem cells (MSCs) can regulate the inflammatory microenvironment, thereby controlling the proliferation, differentiation, and migration of immune cells. Connexin 43(Cx43), a key gap junction protein, has been shown to form gap junctions for communication between neighboring cells.
Objective: We investigated the expression of Cx43 in dermal mesenchymal stem cells (DMSCs) derived from psoriasis patients and explored the relationship between the Cx43-mediated gap junction intercellular communication (GJIC) and DMSCs.
Methods: Human DMSCs were isolated and propagated in adherent culture. Quantitative real-time reverse transcription PCR and western blot and immunofluorescence were used to detect the expression and localization of Cx43 in DMSCs. Fluorescence redistribution after photobleaching was performed to assess adjacent DMSCs GJIC. CCK8 was used to detect the proliferation of DMSCs before and after gap junction blocker (18α-glycyrrhetinic acid; AGA) treatment. Cell energy metabolism was analyzed with an energy metabolism analyzer.
Results: Cx43 was located in the cytoplasm and cytomembrane, as well as partially in the nucleus of DMSCs. The expression of Cx43 in psoriasis DMSCs was higher than that in control samples and the gap junction function was enhanced. In addition, the glycolysis and mitochondrial respiration of psoriasis DMSCs were also enhanced. However, AGA inhibited the expression of Cx43, attenuated GJIC function, and inhibited the proliferation of DMSCs.
Conclusions: Our results indicated that the expression of Cx43 in DMSCs from psoriasis lesions is increased and that the inhibition of Cx43 leads to the inhibition of both GJIC and DMSCs proliferation.
Keywords: Connexin 43; Fluorescent photobleaching recovery; Gap junction intercellular communication; Mesenchymal stem cells; Psoriasis.
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