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Expression and functional regulation of gap junction protein connexin 43 in dermal mesenchymal stem cells from psoriasis patients.
Acta Histochemica ( IF 2.5 ) Pub Date : 2020-04-14 , DOI: 10.1016/j.acthis.2020.151550
Ying Wang 1 , Yanyang Liang 1 , Jiao Li 1 , Ruixia Hou 1 , Junqin Li 1 , Nannan Liang 1 , Jianxiao Xing 1 , Juanjuan Jiao 1 , Wenjuan Chang 1 , Xinhua Li 1 , Kaiming Zhang 1
Affiliation  

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.

中文翻译:

牛皮癣患者真皮间充质干细胞中间隙连接蛋白连接蛋白43的表达和功能调控。

背景技术牛皮癣是一种慢性复发性炎性疾病。间充质干细胞(MSC)可以调节炎症性微环境,从而控制免疫细胞的增殖,分化和迁移。连接蛋白43(Cx43),一种关键的间隙连接蛋白,已经显示出形成间隙连接,用于相邻细胞之间的通讯。目的研究牛皮癣患者皮肤间充质干细胞(DMSCs)中Cx43的表达,探讨Cx43介导的间隙连接细胞间通讯(GJIC)与DMSC之间的关系。方法分离人DMSCs并在贴壁培养中繁殖。实时荧光定量PCR,Western blot和免疫荧光检测DMSCs中Cx43的表达和定位。光漂白后进行荧光重新分配,以评估相邻的DMSCs GJIC。使用CCK8检测间隙连接阻滞剂(18α-甘草次酸; AGA)治疗前后DMSC的增殖。用能量代谢分析仪分析细胞能量代谢。结果Cx43位于DMSCs的细胞质和细胞膜中,以及部分位于细胞核中。牛皮癣DMSCs中Cx43的表达高于对照样品,间隙连接功能增强。另外,牛皮癣DMSCs的糖酵解和线粒体呼吸也得到增强。然而,AGA抑制Cx43的表达,减弱GJIC功能,并抑制DMSC的增殖。
更新日期:2020-04-14
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