전곡류의 섭취와 만성질환의 유병율은 음의 상관관계가 있는 것으로 알려져 있다. 본 연구에서는 선행 연구 결과, 지방축적억제능이 우수한 소재로 선정된 기장의 항염증능 여부를 검증하고자 하였다. 이를 위해 RAW264.7 세포에 기장열수분획(1 ㎍/㎖ 및 10 ㎍/㎖)과 lipopolysaccharide(LPS)를 함께 처리한 후, 24시간 배양시켜 염증매개인자들의 분비량 및 mRNA 발현 정도를 측정하였다. 또한 LPS 자극에 대한 첫 번째 신호전달인자로 알려져 있는 interleukin-1 receptor associated kinase-4(IRAK-4)의 단백질 발현 정도를 측정하였다. 본 연구결과, 기장의 열수분획(10 ㎍/㎖)은 LPS로 유도된 NO, PGE2, TNF-α, IL-6 및 MCP-1의 생성량 및 mRNA 발현량을 유의적으로 억제하였다(p<0.05). 특히 이들 지표 중 pro-inflammatory cytokine인 TNF-α와 IL-6의 mRNA 발현량이 효과적으로 감소하였다(p<0.01). IRAK-4의 단백질 발현량 또한 유의적으로 감소하여 LPS 자극에 대한 기장열수분획의 항염증능은 toll-like receptor(TLR)를 통한 IRAK-4를 매개로 하는 신호전달체계 조절에 기인하는 것으로 사료된다.

14-3-3 is a highly conserved, ubiquitously expressed protein family. It associates with diverse cellular proteins through its specific phosphoserine/phosphothreonine-binding activity and thus contributes to the regulation of crucial cellular processes such as metabolism, signal transduction, cell-cycle control, apoptosis, protein trafficking, transcription and stress responses. This study aims to determine changes in levels of 14-3-3 isoforms and 14-3-3 - associated proteins in Helicobacter pylori(H. pylori)-infected gastric epithelial AGS cells. AGS cells were stimulated with H. pylori(NCTC 11637) at the ratio of 300:1(bacterium:cell). Western blot analysis revealed that 14-3-3 σ was elevated at 3 hr after H. pylori treatment. Other isoforms were not significantly affected by H. pylori infection. Using immunoprecipitation to 14-3-3 σ, followed by proteomic analysis, we found that S phase kinase associated protein isoform 2 bound to 14-3-3 σ has increased. In contrast, three proteins (DEAD-box polypeptide 3, heterogeneous nuclear ribonucleoprotein H2 and WD repeat-containing protein isoform 1) bound to 14-3-3 decreased by H. pylori infection. Our results suggest that 14-3-3 may play an important regulatory role in H. pylori-induced signal transduction in gastric epithelial cells.

Human pituitary tumor transforming gene 1 (PTTG1), which is a newly identified proto-oncogene, is highly expressed in normal pituitary tissues containing proliferating cells and in several cancers. Also, PTTG1 has been known as a securin to involve in the regulation of c ell-cycle and in t he p rogression o f tumor. B u t the effect o f PTTG1 in o ral squamous cell carcinoma (oral SCC) h as not b een studied yet. The objective of this study is to analyze the expression of PTTG1 in oral SCC cell lines (YD-10B and YD-15) and to evaluate the effect of PTTG1 on oral SCC cell lines for the migration effect by PTTG1 siRNA treatment. Western blot, migration assay, and zymography were performed to evaluate the effects of PTTG1 on the expression of MMP-2/-9 and migration activity after PTTG1 siRNA treatment. PTTG1 was expressed in oral SCC cells lines, otherwise, significantly decreased after PTTG1 siRNA treatment. There is no difference in expression of MMP-2 regardless of PTTG1 siRNA treatment. However, the enzyme activity of MMP-9 was significantly decreased. In addition, the migration activities of oral SCC cells were significantly decreased after PTTG1 siRNA treatment (p<0.001). These results suggested that the down-regulated PTTG1 could inhibit the migration of human oral SCC cells through the low MMP-9 expressions. Therefore, these findings provide a useful guideline for the migration mechanism of oral SCC depend on PTTG1 expression.

Oral squamous cell carcinoma (OSCC) is the most common cancer of oral cancers. Recent data suggest that chemokines could be essential players in carcinogenesis and that tumor cells express chemokine receptors and use chemokines to metastasize to the target organ in many malignancies in humans. The aim of this study was to test the hypothesis that expression of SNPs in chemokine, CXCL1 and CXCL2 correlates with oral squamous cell carcinomas in Korean population. The CXCL1 and CXCL2 genotypes were determined in 21 subjects with oral squamous cell carcinoma and 90 control subjects without oral squamous cell carcinoma. The genotypes were determined by direct sequencing. The genotype distribution and allele frequency within the OSCC patients were not significantly different from those of control subjects. But among OSCC subjects, there was significant difference of CXCL1 gene in the degree of nuclear aberration. These findings suggest that CXCL1 -442C/T polymorphism and CXCL2 -264T/C polymorphism are not related to the development of OSCC but polymorphism of CXCL1 gene might have a relation with progression of OSCC in Korean population.

Human β- defensin-2 (hBD-2) is an antimicrobial peptide which is produced by epithelial cells after stimulation with microorganisms or inflammatory mediators. However, little is known as to whether the LPS and nicotine induces the expression of hBD-2 in periodontal l igament (PDL) cells. T he p urpose o f this s tudy was t o investigate t he r oles o f MAPKs pathway o f nicotine a nd L PS-induced hBD-2 expression in PDL cells. The maximal expression of hBD-2 was observed in nicotine 5 mM and LPS 1 μg/ml treated PDL cells. Nicotine and LPS induced the phosphorylation of p38, c-Jun N-terminal kinase 1 and 2 (JNK1/2), and extracellular signal-regulated kinases 1 and 2 (ERK1/2) MAPK. ERK1/2 inhibitor SB203580, p38 inhibitor PD98059, and JNK inhibitor SP600125, blocked the effects of nicotine and LPS on hBD-2 upregulation in PDL cells. These results collectively suggest that hBD-2 is up-regulated in nicotine and LPS-treated PDL cells through activation of p38, ERK and JNK MAPKs pathway. Our data regarding the up-regulation of hBD-2 may help us to understand the antimicrobial mechanism in periodontal disease

Cancer cells are often found in an ischemic condition due to the rapid outgrowth of their vascular supply, and these cells are expected to develop an increased potential for local invasive growth. Since the first steps are characterized by increased motility and invasiveness, expression of molecules involved in cellular adhesion to extracellular matrix (ECM) is increased in the process of cancer cell invasion and metastasis. In this work we explored the molecular characteristics and its regulatory mechanism of hypoxic oral squamous cell carcinoma (OSCC) cells. Our experiment identified that hypoxia increases α5 integrin protein levels through phosphoinositide 3-kinase (PI3K)/Akt pathway in OSCC cells.

EGCG has inhibitory effect on a variety of cancers by inducing apoptosis and cell cycle arrest or inhibiting angiogenesis and metastasis. EGCG has been found to induce apoptosis in salivary gland carcinoma cells. But the potential anti-invasive effect of EGCG in salivary gland cancer has not been studied yet. The aim of this study is to evaluate the effect of EGCG on salivary gland adenocarcinoma SGT cell adhesion and migration to Type I collagen treatment. Western blot, adhesion and migration assay were performed to evaluate the impacts of EGCG on the expression of MMP-2/-9 and its upstream signaling molecules after treatment of type I collagen. SGT cell adhesion to type I collagen is significantly suppressed by EGCG. EGCG decreased expression of β1 integrin, phosphorylation of FAK, MMP-2/-9 compared with type I collagen treatment. In addition, EGCG inhibited the migration of SGT cells treated with type I collagen. These results suggest that EGCG could effectively inhibit the invasion and migration of human SGT cells by downregulating the expression of β1 integrin and MMP-2/-9 and phosphorylation of FAK, Akt, and Erk. Adhesion and migration to type I collagen of SGT cells can be influenced through EGCG.

Embryonic stem (ES) cells are pluripotent cells derived from the inner cell mass cells of blastocyst with the potential to maintain an undifferentiated state indefinitely. Fully characterized ES cell lines express typical stem cell markers, possess high levels of telomerase activity, show normal karyotype and have the potential to differentiate into numerous cell types under in vitro and in vivo conditions. Therefore, ES cells are potentially valuable for the development of cell transplantation therapies for the treatment of various diseases in animals as well as in humans. However, important problems associated with ES cells from in vitro fertilized blastocysts particularly from humans must be resolved before taking up its therapeutic applications. Current techniques for directed differentiation into somatic cell populations remain inefficient and yield heterogeneous cell populations. This review therefore focuses on ES cells with respect to in vitro propagation and differentiation in basic cell and developmental biology for successful use of these cells in therapeutics.

The central granular cell odontogenic tumor is a rare benign odontogenic neoplasm of uncertain hisotogenesis characterized by varying amounts of eosinophilic granular cells and apparently inactive odontogenic epithelium with variable presence of calcified tissue. We present a case of central granular cell odontogenic tumor involving the maxilla of 35-year-old man with immunohistochemical characterization of granular cells. In microscopic view, the granular cells densely packed in sheets and lobules with abundant eosinophilic, granular cytoplasm and eccentric round-to-ovoid nuclei revealed immunoreactivity for vimentin, α1-antitrysin and CD68, and NSE but not for cytokeratin and S-100 protein while the interspersed odontogenic epithelial cells were positive for cytokeratin only. Granular cells also revealed strong PAS staining. Numerous concentric structured round to ovoid calcified aggregates were also noted. The lesion was treated with excision without recurrence for 8 years. Our immuohistochemical staining findings also suggest that the granular cells of central granular cell odontogenic tumor are mesenchymal in origin with possible histiocytic differentiation

Central granular cell odontogenic tumor (CGCOT) is a rare benign odontogenic neoplasm, with approximately 30 cases having been reported. The pathogenesis of CGCOT as well as the designation of this lesion is controversial because of unknown histogenesis of the granular cell. We present an additional case of CGCOT involving the mandible of a 50-year-old Korean man who complained of asymptomatic swelling of the right buccal gingiva. Current lesion is microscopically characterized by densely packed polyhedral granular cells surrounding interspersed islands or strands of odontogenic epithelium. Immunohistochemically, granular cells were positive for Vimentin and CD68, and negative for cytokeratin and S-100. These features support a mesenchymal origin for the granular cells as other results previously reported.

The purpose of this study was to investigate the effect of cytokine-induced osteoclastogenesis on tooth movement related to orthodontic force. We evaluated the cytotoxicity as well as the expression of OPG and RANKL, which influence the homeostasis of bone metabolism. Titanium particles were applied to human periodontal ligament cells and subcultured fourth generation cells. The ALP assay and the MTT assay were used to assess changes in cytotoxicity. After 48 hours, cytotoxicity increased proportionally with the concentration of titanium. With 20 mg, the cytotoxicity was the lowest. R T-PCR was u sed for assessing m R NA l evels of O PG a nd R ANKL; after 96 hours, t he m R NAs of O PG a nd R ANKL increased steeply. A western blot analysis showed that with 20 mg of titanium, the protein expression of OPG increased linearly with time, especially a fter 96 hours, while t he p rotein e xpression o f RANKL d id n ot s how significant changes with titanium processing. Given the increase in OPG expression after the initial cytotoxicity, changes in cytotoxicity with titanium may be attributable to the antagonistic effect of OPG on cytotoxicity

The present study aimed to verify the effects of DFO on PDL cells, with particular emphasis on focusing on osteoblastic differentiation. Its mechanisms related to heme oxygenase-1 (HO-1) pathway were also analyzed. DFO increased the expression of HO-1 and early osteoblastic differentiation markers, such as alkaline phosphatase (ALP) and bone sialoprotein (BSP). DFO upregulated heme oxygenase-1. Treatment with HO-1 siRNA blocked the DFO-stimulated osteoblastic differentiation and HO-1 expression. The NF-kB inhibitor pyrrolidine dithiocarbamate, phosphatidylinositol 3-kinase inhibitor Wortmannin, and p38 MAPK inhibitor U0126 blocked the effects of DFO on HO-1 expression and osteoblastic differentiation in PDL cells. Collectively, these data suggest that DFO promotes osteoblastic differentiation and induces the expression of defense protein HO-1 probably via PI3K, p38 MAPK, and NF-kB signalling pathways in PDL cells.

Previously, we reported that the osmolarity conditions in the satellite region were affected CpG DNA methylation status while Pre-1 sequence was not affected CpG DNA methylation in pNT blastocyst stage. This study was conducted to investigate the DNA methylation status of repeat sequences in pig nuclear transfer (pNT) embryos produced under different osmolarity culture conditions. Control group of pNT embryos was cultured in PZM-3 for six days. Other two treatment groups of pNT embryos were cultured in modified PZM-3 with 138 mM NaCl or 0.05 M sucrose (mPZM-3, 320 mOsmol) for two days, and then cultured in PZM-3 (270 mOsmol) for four days. The DNA methylation status of the Pre-1 sequences in blastocysts was characterized using a bisulfite-sequencing method. Intriguingly, in the present study, we found the unique DNA methylation at several non-CpG sequences at the Pre-1 sequences in all groups. The non-CpG methylation was hypermethylated in all three groups, including in vivo group (86.90% of PZM- 3; 83.87% of NaCl; 84.82% of sucrose; 90.94% of in vivo embryos). To determine whether certain non-CpG methylated sites were preferentially methylated, we also investigated the methylation degree of CpA, CpT and CpC. Excepting in vivo group, preference of methylation was CpT>CpC>CpA in all three groups investigated. These results indicate that DNA methylation of Pre-1 sequences was hypermethylated in CpG as well as non-CpG site, regardless modification of osmolarity in a culture media.