Non-surgical periodontal therapy can effectively improve periodontal, circulating inflammatory and nutritional status in ESRD patients. Non-surgical periodontal therapy, as a relatively simple intervention, has beneficial systemic effects in ESRD patients.

Depending on a biofilm lifestyle, Streptococcus mutans (S. mutans) is thought to be one of the primary causative agents of dental caries. Biofilm formation and adhesion are crucial physiological functions and virulence factors for S. mutans. Thus, attempts to control the development of dental caries only by inhibiting one of the several virulence factors are not effective. Cyclic diguanylate (c-di-GMP) [bis(3',5')-cyclic diguanylic acid] is a prokaryotic cyclic dinucleotide second messenger that has been implicated in determining the timing and amplitude of complex biological processes from biofilm formation and virulence to photosynthesis. Here, we demonstrate that this signaling molecule also plays a role in the ability of S. mutans to initiate biofilm formation and adhere to tooth surfaces. To test this hypothesis, S. mutans UA159 and its gcp gene knockout mutant were assayed for their ability to initiate biofilm formation and adherence. The spatial distribution and architecture of the biofilms were examined by scanning electron microscopy. These results show that inactivation of the gcp gene resulted in the formation of an abnormal biofilm. We confirmed that c-di-GMP was effective in preventing biofilm formation of S. mutans UA159. We also found that extracellular c-di-GMP inhibited the adherence of S. mutans to tooth surfaces and reduced (>50%) biofilm formation compared to the untreated control. These results indicate that c-di-GMP attenuates the caries-inducing virulence factors of S. mutans. This suggests that c-di-GMP may be used alone or in combination with other antimicrobial agents, and that such a treatment could be developed into a novel method to prevent tooth decay.

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Malignant glioma is the most prevalent form of malignant brain tumor. Although radiotherapy is widely used in glioma treatment, the radioresistance of glioma cells limits the success of the glioma treatment. The lack of effective targets and signaling pathways to reverse glioma radioresistance is the critical obstacle in successful treatment. In this study, we demonstrate that mitochondrial ATP-sensitive potassium channels (mtK(ATP) channels) are overexpressed in glioma cells and are closely related to the malignancy grade and the overall survival of the patients. Importantly, we showed that mtK(ATP) channels could control glioma radioresistance by regulating reactive oxygen species (ROS)-induced ERK activation. The inhibition of mtK(ATP) channels suppresses glioma radioresistance by inhibiting ERK activation both in vitro and in vivo. These findings reveal the important roles of the mitochondria and mtK(ATP) channels as key regulators in the radioresistance of glioma cells, and suggest that mtK(ATP) channel blockers and MAPK/ERK kinase (MEK) inhibitors are potential targets for drug development of glioma treatments.

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Tooth formation is tightly regulated by epithelial-mesenchymal interactions via hierarchic cascades of signaling molecules. The glycosaminoglycan (GAG) chains covalently attached to the core protein of proteoglycans (PGs) provide docking sites for signaling molecules and their receptors during the morphogenesis of tissues and organs. While PGs are believed to play important roles in tooth formation, little is known about their exact functions in this developmental process and the relevant molecular basis. Family with sequence similarity member 20-B (FAM20B) is a newly identified kinase phosphorylating the xylose in the common linkage region connecting the GAG with the protein core of PGs. The phosphorylation of xylose is essential to the common linkage elongation and the subsequent GAG assembly. In this study, we generated Fam20B-floxed allele in mice and found that inactivating Fam20B in the dental epithelium leads to supernumerary maxillary and mandibular incisors. This finding highlights the pivotal role of PGs in tooth morphogenesis and opens a new window for understanding the regulatory mechanism of PG-mediated signaling cascades during tooth formation.

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