• Journal of Gastric Cancer
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• 제13권4호
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• pp.232-241
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• 2013

Purpose: Gastrokine 1 plays an important role in gastric mucosal defense. Additionally, the Gastrokine 1-miR-185-DNMT1 axis has been shown to suppress gastric carcinogenesis through regulation of epigenetic alteration. Here, we investigated the effects of Gastrokine 1 on DNA methylation and gastritis. Materials and Methods: Expression of Gastrokine 1, DNMT1, EZH2, and c-Myc proteins, and the presence of Helicobacter pylori CagA protein were determined in 55 non-neoplastic gastric mucosal tissue samples by western blot analysis. The CpG island methylation phenotype was also examined using six markers (p16, hMLH1, CDH1, MINT1, MINT2 and MINT31) by methylation-specific polymerase chain reaction. Histological gastritis was assessed according to the updated Sydney classification system. Results: Reduced Gastrokine 1 expression was found in 20 of the 55 (36.4%) gastric mucosal tissue samples and was closely associated with miR-185 expression. The Gastrokine 1 expression level was inversely correlated with that of DNMT1, EZH2, and c-Myc, and closely associated with the degree of gastritis. The H. pylori CagA protein was detected in 26 of the 55 (47.3%) gastric mucosal tissues and was positively associated with the expression of DNMT1, EZH2, and c-Myc. In addition, 30 (54.5%) and 23 (41.9%) of the gastric mucosal tissues could be classified as CpG island methylation phenotype-low and CpG island methylation phenotype-high, respectively. Reduced expression of Gastrokine 1 and miR-185, and increased expression of DNMT1, EZH2, and c-Myc were detected in the CpG island methylation phenotype-high gastric mucosa. Conclusions: Gastrokine 1 has a crucial role in gastric inflammation and DNA methylation in gastric mucosa.

• 한국콘텐츠학회논문지
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• 제16권10호
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• pp.435-442
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• 2016

전 세계적으로 비만인구의 증가로 인해 경제적 부담이 확대되고 있으며, 그 원인으로 육체적 활동의 감소 및 식이관리의 실패가 손꼽히고 있다. 영양성분 및 칼로리를 기반으로 한 맞춤 식단정보 제공 시스템과는 차별적으로 본 연구는 개인 맞춤형 기능성 식품을 추천하기 위해 비만 관련 SNP (single nucleotide polymorphism) 정보를 활용하였다. 본 연구를 위해 GWAS (Genome-wide association study) 분석을 수행하여 한국인 특이적인 비만 관련 SNP을 발굴하고, 이를 활용하여 유전적 정보를 입력하여 SNP genoype-phenoype 정보에 따른 맞춤 식단옴을 추천하였다. 또한 USDA (The United States Department of Agriculture) 식품 정보를 활용할 수 있도록 식품 통합 Database를 구축하여 식단 추천에 적용하였다. 그 결과, 표현형 정보 BMI (Body Mass Index)는 정상 수치를 가지고 있으나, 비만 관련 SNP 정보를 가지고 있는 샘플은 유전적 비만 위험도를 나타내어 식이관리가 필요하다는 정보를 확인하였으며, 관련 식품 정보를 제공하였다. 따라서 표현형에 따른 비만에 관한 정보와 유전형 정보가 일치하는 것은 아니며, 이는 표현형적 정보만을 이용한 비만 관리 식이 추천에는 한계가 있음을 의미하며 이러한 결과는 비만외 다른 성인병들에도 적용이 필요하며 이를 위해서는 표현형-유전적 통합정보를 기반 한 맞춤식이 추천이 필요함을 나타내었다.

• 미생물학회지
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• 제53권3호
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• pp.149-155
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• 2017

대부분의 Proteobacteria에 존재하는 질소 인산전달계는 다양한 세포내 조절에 관여하는 cascade이다. 이들은 ptsP 유전자에 의해 암호화되는 $EI^{Ntr}$, ptsO에 의해 암호화되는 NPr, ptsN에 의해 암호화되는 $EIIA^{Ntr}$로 이루어져 있다. 이들 중 $EIIA^{Ntr}$은 $K^+$ 농도 조절, ppGpp 농도 조절, 질소와 탄소 대사, ABC transporter의 조절 등 다양한 세포내 조절과정에 관여하지만, NPr의 생리적 기능에 대해서는 알려진 바가 많지 않다. 최근의 한 논문은 대장균에서 탈인산화된 NPr이 세포막 스트레스 반응에 관여한다는 사실이 밝혔다. 본 연구에서는 NPr과 관련된 새로운 표현형을 제공한다. ptsP 유전자가 결손된 균주는 filamentation 표현형을 나타내었다. ptsP 결손균주의 이런 표현형은 ptsO 유전자의 추가적인 결실에 의해 사라졌지만, ptsN 유전자의 추가적 소실에 의해서는 유지되었다. 이는 ptsP 결손균주의 filamentation 표현형이 탈인산화된 NPr의 증가 때문에 나타났음을 나타낸다. 이런 생각은 야생종에서 탈인산화된 NPr이 증가되었을 때 filamentation 표현형을 나타낸다는 사실을 통해 확증되었다. 또한 탈인산화된 NPr의 양이 증가함에 따라 대장균의 세포 길이가 점진적으로 증가한다는 사실을 알 수 있었다. 이러한 결과는 탈인산화된 NPr이 대장균의 형태적 변화를 유도함을 시사한다.

• Molecules and Cells
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• 제39권6호
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• pp.468-476
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• 2016

PLZF-expressing invariant natural killer T cells and CD4 T cells are unique subsets of innate T cells. Both are selected via thymocyte-thymocyte interaction, and they contribute to the generation of activated/memory-like CD4 and CD8 T cells in the thymus via the production of IL-4. Here, we investigated whether $PLZF^+$ innate T cells also affect the development and function of $Foxp3^+$ regulatory CD4 T cells. Flow cytometry analysis of the thymus and spleen from both CIITA transgenic C57BL/6 and wild-type BALB/c mice, which have abundant $PLZF^+$ CD4 T cells and invariant natural killer T cells, respectively, revealed that $Foxp3^+$ T cells in these mice exhibited a $CD103^+$ activated/memorylike phenotype. The frequency of $CD103^+$ regulatory T cells was considerably decreased in $PLZF^+$ cell-deficient $CIITA^{Tg}Plzf^{lu/lu}$ and $BALB/c.CD1d^{-/-}$ mice as well as in an IL-4-deficient background, such as in $CIITA^{Tg}IL-4^{-/-}$ and $BALB/c.IL-4^{-/-}$ mice, indicating that the acquisition of an activated/ memory-like phenotype was dependent on $PLZF^+$ innate T cells and IL-4. Using fetal thymic organ culture, we further demonstrated that IL-4 in concert with TGF-${\beta}$ enhanced the acquisition of the activated/memory-like phenotype of regulatory T cells. In functional aspects, the activated/ memory-like phenotype of Treg cells was directly related to their suppressive function; regulatory T cells of $CIITA^{Tg}PIV^{-/-}$ mice more efficiently suppressed ovalbumin-induced allergic airway inflammation compared with their counterparts from wild-type mice. All of these findings suggest that $PLZF^+$ innate T cells also augmented the generation of activated/memory-like regulation via IL-4 production.

• BMB Reports
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• 제55권11호
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• pp.565-570
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• 2022

Pulmonary arterial hypertension (PAH) is a progressive and devastating disease whose pathogenesis is associated with a phenotypic switch of pulmonary arterial vascular smooth muscle cells (PASMCs). Bone morphogenetic protein (BMP) signaling and potassium two pore domain channel subfamily K member 3 (KCNK3) play crucial roles in PAH pathogenesis. However, the relationship between BMP signaling and KCNK3 expression in the PASMC phenotypic switching process has not been studied. In this study, we explored the effect of BMPs on KCNK3 expression and the role of KCNK3 in the BMP-mediated PASMC phenotypic switch. Expression levels of BMP receptor 2 (BMPR2) and KCNK3 were downregulated in PASMCs of rats with PAH compared to those in normal controls, implying a possible association between BMP/BMPR2 signaling and KCNK3 expression in the pulmonary vasculature. Treatment with BMP2, BMP4, and BMP7 significantly increased KCNK3 expression in primary human PASMCs (HPASMCs). BMPR2 knockdown and treatment with Smad1/5 signaling inhibitor substantially abrogated the BMP-induced increase in KCNK3 expression, suggesting that KCNK3 expression in HPASMCs is regulated by the canonical BMP-BMPR2-Smad1/5 signaling pathway. Furthermore, KCNK3 knockdown and treatment with a KCNK3 channel blocker completely blocked BMP-mediated anti-proliferation and expression of contractile marker genes in HPAMSCs, suggesting that the expression and functional activity of KCNK3 are required for BMP-mediated acquisition of the quiescent PASMC phenotype. Overall, our findings show a crosstalk between BMP signaling and KCNK3 in regulating the PASMC phenotype, wherein BMPs upregulate KCNK3 expression and KCNK3 then mediates BMP-induced phenotypic switching of PASMCs. Our results indicate that the dysfunction and/or downregulation of BMPR2 and KCNK3 observed in PAH work together to induce aberrant changes in the PASMC phenotype, providing insights into the complex molecular pathogenesis of PAH.

• Bulletin of the Korean Chemical Society
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• 제32권11호
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• pp.4137-4140
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• 2011

• 한국미생물학회:학술대회논문집
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• 한국미생물학회 2005년도 International Meeting of the Microbiological Society of Korea
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• pp.227.3-227
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• 2005

• 한국동물학회:학술대회논문집
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• 한국동물학회 1998년도 한국생물과학협회 학술발표대회
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• pp.330.1-330
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• 1998

No Abstract, See Full Text

• 한국동물학회:학술대회논문집
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• 한국동물학회 1998년도 한국생물과학협회 학술발표대회
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• pp.326.2-326
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• 1998

No Abstract, See Full Text

• 한국환경성돌연변이발암원학회:학술대회논문집
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• 한국환경성돌연변이발암원학회 2002년도 Molecular and Cellular Response to Toxic Substances
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• pp.141-141
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• 2002