Detection of mesenteric ischemia by means of endoscopic visible light spectroscopy after luminal feeding

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Expression analysis of α-smooth muscle actin and tenascin-C in the periodontal ligament under orthodontic loading or in vitro culture

α-smooth muscle actin (α-SMA) and tenascin-C are stress-induced phenotypic features of myofibroblasts. The expression levels of these two proteins closely correlate with the extracellular mechanical microenvironment. We investigated how the expression of α-SMA and tenascin-C was altered in the periodontal ligament (PDL) under orthodontic loading to indirectly reveal the intrinsic mechanical microenvironment in the PDL. In this study, we demonstrated the synergistic effects of transforming growth factor-β1 (TGF-β1) and mechanical tensile or compressive stress on myofibroblast differentiation from human periodontal ligament cells (hPDLCs). The hPDLCs under higher tensile or compressive stress significantly increased their levels of α-SMA and tenascin-C compared with those under lower tensile or compressive stress. A similar trend was observed in the tension and compression areas of the PDL under continuous light or heavy orthodontic load in rats. During the time-course analysis of expression, we observed that an increase in α-SMA levels was matched by an increase in tenascin-C levels in the PDL under orthodontic load in vivo. The time-dependent variation of α-SMA and tenascin-C expression in the PDL may indicate the time-dependent variation of intrinsic stress under constant extrinsic loading.     

牙周膜干细胞对口腔表皮样癌KB细胞增殖影响的研究

目的探讨牙周膜干细胞(periodontal ligament stem cells,PDLSCs)对口腔表皮样癌细胞系KB细胞增殖的影响及其机制。方法取拔除的阻生第三磨牙和正畸减数牙,采用酶消化法分离PDLSCs。应用Transwell培养小室将PDLSCs和KB细胞以不同的比例混合培养,建立共培养体系。48h后,应用MTT法观察KB细胞增殖情况。在部分实验的培养体系中加入抗IL-6抗体,同法观察KB细胞增殖。收集共培养48h的KB细胞,通过流式细胞术检测其凋亡情况,RT-PCR法检测其Caspase-3的表达,蛋白质印迹法检测其β-catenin表达情况。收集PDLSCs,采用RT-PCR法检测其IL-6的表达。结果 PDLSCs与KB细胞共培养48h,PDLSCs∶KB细胞数量比为1∶1时,吸光度值为1.33±0.18,与单独KB细胞组的2.65±0.33相比,差异有统计学意义,P=0.041;PDLSCs∶KB细胞数量比为5∶1时,吸光度值为1.06±0.18,与单独KB细胞组相比,差异有统计学意义,P=0.001。表明PDLSCs能够显著抑制KB细胞的增殖。PDLSCs∶KB细胞数量比为1∶1时,KB细胞的凋亡率为(39±5)%,与单独KB细胞组的(15±4)%相比,P=0.022;PDLSCs∶KB细胞数量比为5∶1时,KB细胞的凋亡率为(51±7)%,与单独KB细胞组相比,P=0.001。在PDLSCs与KB细胞的共培养体系中,加入抗IL-6抗体后,PDLSCs抑制KB细胞的增殖作用显著减轻。RT-PCR实验发现,共培养48h后的PDLSCs的IL-6表达升高。蛋白质印迹法检测结果发现,培养48h后的KB细胞β-catenin表达无明显变化。结论 PDLSCs能抑制口腔表皮样癌KB细胞的增殖和促进KB细胞凋亡。     

Mechanisms of orofacial sensory processing in the rat insular cortex

Background

Orofacial structures involve multifarious organs, including the lips, tongue, soft and hard palates, teeth, periodontal ligaments, salivary glands, and facial skin. These organs process multiple types of sensory information that contributes to performance of the finely regulated orofacial movements. Among the types of sensory information, gustation is processed in the insular cortex, and, thus, part of the insular cortex is called the gustatory cortex. Moreover, the insular cortex receives not only gustatory information but also information on other somatosensory and chemical sensations, including nociception, thermoreception, audition, and olfaction.

Jumonji domain-containing protein 3 regulates the early inflammatory response epigenetically in human periodontal ligament cells

ObjectiveTo investigate the role of the histone 3 lysine 27 trimethylation (H3K27me3) demethylase Jumonji domain-containing protein 3 (Jmjd3) in the epigenetic regulation of the inflammatory response in human periodontal ligament cells (HPDLs).DesignHPDLs were stimulated with lipopolysaccharide from E. coli. The expression of Jmjd3 in HPDLs was examined by quantitative real-time polymerase chain reaction (Q-PCR), Western Blot and immunofluorescent staining. Potential target genes were selected by silencing Jmjd3 and were confirmed by Chromatin Immunoprecipitation (ChIP).ResultsQ-PCR, Western Blot and immunofluorescent staining revealed that the expression of Jmjd3 was increased in inflamed HPDLs. Knockdown of Jmjd3 led to the suppression of inflammation-induced up-regulation of interleukin-6 and interleukin-12. Moreover, ChIP assays demonstrated that Jmjd3 was recruited to the promoters of interleukin-6 and interleukin-12b and this recruitment was associated with decreased levels of trimethylated histone 3 lysine 27 (H3K27).ConclusionsIt was concluded that Jmjd3 regulated the activation of interleukin-6 and interleukin-12b in the early inflammatory response of HPDLs via demethylation of H3K27me3 at promoters. This molecular event may play an important role in the regulation of the inflammatory response in HPDLs.