• 치위생과학회지
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• 제14권2호
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• pp.87-93
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• 2014

Dental plaque resides passively at a site and makes an active contribution to the maintenance of health. The bacterial composition of plaque remains relatively stable despite regular exposure to minor environmental stress. This stability, homeostasis is due to a dynamic balance of microbial interactions. However, the homeostasis can break down, leading to shifts in the balance of the microflora. This change can be a sign of initial dental caries. It is proposed that disease can be prevented or treated not only by targeting the putative pathogens but also by interfering with the processes that drive the breakdown in homeostasis. It is essential to understand the plaque as a mixed species biofilm. In this essay I reviewed an extension of the caries ecological hypothesis to explain the relation between dynamic changes in the phenotypic/genotypic properties of plaque bacteria and the demineralization and remineralization balance of the dental caries process. We will have the strategies to impact significantly on clinical practice as understanding dental biofilm.

• BMB Reports
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• 제46권10호
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• pp.479-483
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• 2013

The balance between osteoblast-dependent bone formation and osteoclast-dependent bone resorption maintains bone homeostasis. In inflammatory conditions, this balance shifts toward bone resorption, causing osteolytic bone lesions observed in rheumatoid arthritis and periodontitis. A recently discovered family of cytokine IL-17 is widely reported to mediate diverse inflammatory processes. During the last decade, novel roles for IL-17 in skeletal homeostasis have been discovered indicating the potential importance of this cytokine in bone metabolism. This review will summarize and discuss the involvement of IL-17 during bone homeostasis in both physiologic and pathologic conditions. A better understanding of the role of IL-17 in skeletal systems warrants an advance in bone biology, as well as development of therapeutic strategies against bone-lytic diseases, such as rheumatoid arthritis and periodontitis.

• Clinical and Experimental Pediatrics
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• 제50권3호
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• pp.223-229
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• 2007

The fetus is completely dependent on mother for glucose and other nutrient transfer across the placenta. At birth, when the maternal supply is discontinued, the neonate must adjust to an independent existence. The changes in the neonate's glucose homeostasis during this transition to the extrauterine environment are influenced by the mother's metabolism and intrinsic fetal and placental problems. Maturation of carbohydrate homeostasis results from a balance between substrate availability and coordination of developing hormonal, enzymatic, and neural systems. These mechanisms may not be fully developed in neonates, so the neonate is vulnerable to carbohydrate disequilibrium resulting in damage to the central nervous system. Hypoglycemia is a relatively common metabolic problem seen during newborn care. However its definition, management and long term sequalae remain controversial. Hyporglycemia occurs frequently as a transient disorder with excellent prognosis. It also may persist and recur and cause permanent neurological complications. Although the key to effective treatment of hypoglycemia is diagnostic specific, the maintenance of euglycemia is critical to the preservation of central nervous system function. This article discusses physiology of perinatal glucose homeostasis, focusing on evaluation and treatment of hypoglycemia.

• Clinical and Experimental Pediatrics
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• 제50권3호
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• pp.230-235
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• 2007

In the early neonatal period, the neonate is challenged by the loss of the placental calcium transport and manifests a quick transition, from an environment in which PTHrP plays an important role to a PTH- and 1,25-dihydroxyvitamin D-controlled neonatal milieu. Disturbances in mineral homeostasis are common in the neonatal period, especially in premature infants and infants who are hospitalized in an intensive care unit. In many cases these disturbances are thought to be exaggerated responses to the normal physiological transition from the intrauterine environment to neonatal independence. Some disturbances in calcium and phosphate homeostasis are the result of genetic defects, which in many instances can now be identified at the molecular level. Although fetus develop remarkably normally in the presence of maternal calcium, PTH and vitamin D deficiency, the neonates demonstrate abnormalities that are consequences of the prior abnormal maternal calcium homeostasis. Evaluation and management of hypocalcemia and hypercalcemia in neonate requires specific knowledge of perinatal mineral physiology and the unique clinical and biochemical features of newborn mineral metabolism.

• Molecules and Cells
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• 제25권1호
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• pp.124-130
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• 2008

Astrocyte ion channels participate in ionic homeostasis in the brain. Inward rectifying potassium channels (Kir channels) in astrocytes have been particularly implicated in $K^+$ homeostasis because of their high open probability at resting potential and their increased conductance at high concentrations of extracellular $K^+$. We examined the expression of the Kir2.1 subunit, one of the Kir channel subunits, in the mouse brain by immunohistochemistry. Kir2.1 channels were widely distributed throughout the brain, with high expression in the olfactory bulb and the cerebellum. Interestingly, they were abundantly expressed in astrocytes of the olfactory bulb, while astrocytes in other brain regions including the hippocampus did not show any detectable expression. However, Kir2.1 channel-expressing cells were dramatically increased in the hippocampus by kainic acid-induced seizure and the cells were glial fibrillary acidic protein (GFAP)-positive, which confirms that astrocytes in the hippocampus express Kir2.1 channels under pathological conditions. Our results imply that Kir2.1 channels in astrocyte may be involved in buffering $K^+$ against accumulated extracellular $K^+$ caused by neuronal hyperexcitability under phathophysiological conditions.

• BMB Reports
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• 제50권4호
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• pp.162-163
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• 2017

RNA polymerase II-interacting the Set2 methyltransferase co-transcriptionally methylates histone H3 at lysine 36 within the body of genes. This modification facilitates histone deacetylation by Rpd3S HDAC in 3' transcribed regions to suppress cryptic initiation and slow elongation. Although this pathway is important for global deacetylation, no strong effects have been seen on genome-wide transcription under optimized laboratory conditions. In contrast, this pathway slows the kinetics of mRNA induction when target genes are induced upon environmental changes. Interestingly, a majority of Set2-repressed genes are overlapped by a lncRNA transcription that targets H3K36 methylation and deacetylation by Rpd3S HDAC to mRNA promoters. Furthermore, this pathway delays the induction of many cryptic transcripts upon environmental changes. Therefore, the Set2-Rpd3S HDAC pathway functions to fine-tune expression dynamics of mRNAs and ncRNAs.

• Molecules and Cells
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• 제37권10호
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• pp.747-752
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• 2014

Protein kinase C (PKC) family members phosphorylate a wide variety of protein targets and are known to be involved in diverse cellular signaling pathways. However, the role of PKC in receptor activator of NF-${\kappa}B$ ligand (RANKL) signaling has remained elusive. We now demonstrate that $PKC{\beta}$ acts as a positive regulator which inactivates glycogen synthase kinase-$3{\beta}$ (GSK-$3{\beta}$) and promotes NFATc1 induction during RANKL-induced osteoclastogenesis. Among PKCs, $PKC{\beta}$ expression is increased by RANKL. Pharmacological inhibition of $PKC{\beta}$ decreased the formation of osteoclasts which was caused by the inhibition of NFATc1 induction. Importantly, the phosphorylation of GSK-$3{\beta}$ was decreased by $PKC{\beta}$ inhibition. Likewise, down-regulation of $PKC{\beta}$ by RNA interference suppressed osteoclast differentiation, NFATc1 induction, and GSK-$3{\beta}$ phosphorylation. The administration of PKC inhibitor to the RANKL-injected mouse calvaria efficiently protected RANKL-induced bone destruction. Thus, the $PKC{\beta}$ pathway, leading to GSK-$3{\beta}$ inactivation and NFATc1 induction, has a key role in the differentiation of osteoclasts. Our results also provide a further rationale for $PKC{\beta}$'s therapeutic targeting to treat inflammation-related bone diseases.

• Molecules and Cells
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• 제37권6호
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• pp.487-496
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• 2014

Angiotensinogen (AGT), the precursor of angiotensin I, is known to be involved in tumor angiogenesis and associated with the pathogenesis of coronary atherosclerosis. This study was undertaken to determine the role played by AGT in endothelial progenitor cells (EPCs) in tumor progression and metastasis. It was found that the number of EPC colonies formed by AGT heterozygous knockout ($AGT^{+/-}$) cells was less than that formed by wild-type (WT) cells, and that the migration and tube formation abilities of $AGT^{+/-}$ EPCs were significantly lower than those of WT EPCs. In addition, the gene expressions of vascular endothelial growth factor (VEGF), Flk1, angiopoietin (Ang)-1, Ang-2, Tie-2, stromal derived factor (SDF)-1, C-X-C chemokine receptor type 4 (CXCR4), and of endothelial nitric oxide synthase (eNOS) were suppressed in $AGT^{+/-}$ EPCs. Furthermore, the expressions of hypoxia-inducible factor (HIF)-$1{\alpha}$and $-2{\alpha}$ were downregulated in $AGT^{+/-}$ early EPCs under hypoxic conditions, suggesting a blunting of response to hypoxia. Moreover, the activation of Akt/eNOS signaling pathways induced by VEGF, epithelial growth factor (EGF), or SDF-$1{\alpha}$ were suppressed in $AGT^{+/-}$ EPCs. In $AGT^{+/-}$ mice, the incorporation of EPCs into the tumor vasculature was significantly reduced, and lung tumor growth and melanoma metastasis were attenuated. In conclusion, AGT is required for hypoxia-induced vasculogenesis.

• Journal of Microbiology and Biotechnology
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• 제22권6호
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• pp.742-753
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• 2012

Copper-containing compounds are introduced into the environment through agricultural chemicals, mining, and metal industries and cause severe detrimental effects on ecosystems. Certain microorganisms exposed to these stressors exhibit molecular mechanisms to maintain intracellular copper homeostasis and avoid toxicity. We have previously reported that the soil bacterial isolate Achromobacter sp. AO22 is multi-heavy metal tolerant and exhibits a mer operon associated with a Tn21 type transposon. The present study reports that AO22 also hosts a unique cop locus encoding copper homeostasis determinants. The putative cop genes were amplified from the strain AO22 using degenerate primers based on reported cop and pco sequences, and a constructed 10,552 base pair contig (GenBank Accession No. GU929214). BLAST analyses of the sequence revealed a unique cop locus of 10 complete open reading frames, designated copSRABGOFCDK, with unusual separation of copCD from copAB. The promoter areas exhibit two putative cop boxes, and copRS appear to be transcribed divergently from other genes. The putative protein CopA may be a copper oxidase involved in export to the periplasm, CopB is likely extracytoplasmic, CopC may be periplasmic, CopD is cytoplasmic/inner membrane, CopF is a P-type ATPase, and CopG, CopO, and CopK are likely copper chaperones. CopA, B, C, and D exhibit several potential copper ligands and CopS and CopR exhibit features of two-component regulatory systems. Sequences flanking indicate the AO22 cop locus may be present within a genomic island. Achromobacter sp. strain AO22 is thus an ideal candidate for understanding copper homeostasis mechanisms and exploiting them for copper biosensor or biosorption systems.

• Journal of Ginseng Research
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• 제44권4호
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• pp.580-592
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• 2020

Background: Radix et Rhizoma Ginseng (thereafter called ginseng) has been used as a medicinal herb for thousands of years to maintain people's physical vitality and is also a non-organ-specific cancer preventive and therapeutic traditional medicine in several epidemiologic and preclinical studies. Owing to few toxic side effects and strong enhancement on body immunity, ginseng has admirable application potential and value in cancer chemoprevention. The study aims at investigating the chemopreventive effects of ginseng on cutaneous carcinoma and the underlying mechanisms. Methods: The mouse skin cancer model was induced by 7,12-dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol-13-acetate. Ultraperformance liquid chromatography/mass spectrometry was used for identifying various ginsenosides, the main active ingredients of ginseng. Comprehensive approaches (including network pharmacology, bioinformatics, and experimental verification) were used to explore the potential targets of ginseng. Results: Ginseng treatment inhibited cutaneous carcinoma in terms of initiation and promotion. The content of Rb1, Rb2, Rc, and Rd ginsenosides was the highest in both mouse blood and skin tissues. Ginseng and its active components well maintained the redox homeostasis and modulated the immune response in the model. Specifically, ginseng treatment inhibited the initiation of skin cancer by enhancing T-cell-mediated immune response through upregulating HSP27 expression and inhibited the promotion of skin cancer by maintaining cellular redox homeostasis through promoting nuclear translocation of Nrf2. Conclusion: According to the study results, ginseng can be potentially used for cutaneous carcinoma as a chemopreventive agent by enhancing cell-mediated immunity and maintaining redox homeostasis with multiple components, targets, and links.