Publications by authors named "Seung Yeon Oh"

5 Publications

  • Page 1 of 1

The anti-diabetic effects of NAG-1/GDF15 on HFD/STZ-induced mice.

Sci Rep 2021 Jul 22;11(1):15027. Epub 2021 Jul 22.

Laboratory of Signal Transduction, College of Veterinary Medicine and Research Institute for Veterinary Science, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, South Korea.

Nonsteroidal anti-inflammatory drug-activated gene-1 (NAG-1) plays a role in various diseases. Here, the anti-diabetic effects of NAG-1 were evaluated using a high-fat diet/streptozotocin-induced diabetic mouse model. NAG-1-overexpressing transgenic (NAG-1 Tg) mice exhibited lower body weight, fasting blood glucose levels, and serum insulin levels than wild-type (WT) mice. The homeostatic model assessment of insulin resistance scores of NAG-1 Tg mice were lower than those of WT mice. Hematoxylin and eosin staining revealed a smaller lipid droplet size in the adipose tissues, lower lipid accumulation in the hepatocytes, and larger beta cell area in the pancreas of NAG-1 Tg mice than in those of WT mice. Immunohistochemical analysis revealed downregulated expression of cleaved caspase-3, an apoptosis marker, in the beta cells of NAG-1 Tg mice. Adiponectin and leptin mRNA levels were upregulated and downregulated in NAG-1 Tg mice, respectively. Additionally, the expression of IRS1/PI3K/AKT signaling pathway components, especially Foxo1, which regulates gluconeogenesis in the muscle and white adipose tissue, was downregulated in NAG-1 Tg mice. Furthermore, NAG-1 overexpression promoted the expression of As160 in both muscles and adipocytes, and the mRNA levels of the NLRP3 pathway members were downregulated in NAG-1 Tg mice. Our findings suggest that NAG-1 expression alleviates diabetes in mice.
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http://dx.doi.org/10.1038/s41598-021-94581-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8298384PMC
July 2021

Colorimetric detection of Co2+ ion using silver nanoparticles with spherical, plate, and rod shapes.

Langmuir 2013 Jul 3;29(28):8978-82. Epub 2013 Jul 3.

Department of Chemical Engineering, Kwangwoon University, Nowon-gu, Seoul 139-701, Republic of Korea.

A highly sensitive colorimetric sensing platform for the selective trace analysis for Co(2+) ions is reported, based on glutathione (GSH)-modified silver nanoparticles (AgNP). The shape of metallic nanoparticles used in colorimetric detection, using the unique optical properties of plasmonic nanoparticles, is almost spherical. Therefore, in this work we attempted to investigate the selective detection of heavy metal ion (Co(2+)), with the shape of AgNPs (nanosphere, nanoplate, and nanorod). GSH-AgNP with spherical shape shows a high sensitivity for all of the metal ions (Ni(2+), Co(2+), Cd(2+), Pb(2+), and As(3+)) but poor selective recognition for target metal ions. Whereas, AgNPs solution containing rod-type GSH-AgNP has a special response to Co(2+), and its selective detection might be based on the cooperative effect of CTAB and GSH. Therefore, Co(2+) ion could be selectively recognized using rod-type GSH-AgNPs.
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http://dx.doi.org/10.1021/la401408fDOI Listing
July 2013

Luteolin exerts anti-tumor activity through the suppression of epidermal growth factor receptor-mediated pathway in MDA-MB-231 ER-negative breast cancer cells.

Food Chem Toxicol 2012 Nov 20;50(11):4136-43. Epub 2012 Aug 20.

Department of Food and Nutrition, Sookmyung Women's University, Seoul 140-742, Republic of Korea.

This study investigated the inhibitory effect of luteolin on MDA-MB-231 estrogen receptor (ER) negative breast tumor growth both in vitro and in vivo. Study results showed that luteolin suppresses (3)H thymidine incorporation indicating cell growth inhibition, and this was accompanied by cell cycle arrest at the G2/M and S stages and apoptotic activity. Further analyses showed that luteolin exhibited cell cycle arrest and apoptotic activity by decreasing AKT, PLK1, cyclin B(1), cyclin A, CDC2, CDK2, and Bcl-xL expression and increasing p21 and Bax expression. Underlying mechanisms of action exerted by luteolin included the down-regulation. EGFR mRNA expression followed by the inhibition of EGF-induced MAPK activation, including the phosphorylation of ERK, p38 and AKT. Luteolin-supplementation at 0.01% or 0.05% significantly reduced tumor burden in nude mice inoculated with MDA-MB-231 cells. In conclusion, luteolin effectively suppresses MDA-MB-231 ER-negative breast cancer cell growth, and its anticancer activity may be partly derived from inhibitory effects on EGFR-mediated cell survival.
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http://dx.doi.org/10.1016/j.fct.2012.08.025DOI Listing
November 2012

Modulatory effects of alpha- and gamma-tocopherols on 4-hydroxyestradiol induced oxidative stresses in MCF-10A breast epithelial cells.

Nutr Res Pract 2009 30;3(3):185-91. Epub 2009 Sep 30.

Department of Food and Nutrition, Sookmyung Women's University, 52 Hyochangwon-gil, Yongsan-gu, Seoul 140-742, Korea.

The elevated level of circulating estradiol increases the risk of breast tumor development. To gain further insight into mechanisms involved in their actions, we investigated the molecular mechanisms of 4-hydroxyestradiol (4-OHE(2)) to initiate and/or promote abnormal cell growth, and of alpha- or gamma-tocopherol to inhibit this process. MCF-10A, human breast epithelial cells were incubated with 0.1 microM 4-OHE(2), either with or without 30 microM tocopherols for 96 h. 4-OHE(2) caused the accumulation of intracellular ROS, while cellular GSH/GSSG ratio and MnSOD protein levels were decreased, indicating that there was an oxidative burden. 4-OHE(2) treatment also changed the levels of DNA repair proteins, BRCA1 and PARP-1. gamma-Tocopherol suppressed the 4-OHE(2)-induced increases in ROS, GSH/GSSG ratio, and MnSOD protein expression, while alpha-tocopherol up-regulated BRCA1 and PARP-1 protein expression. In conclusion, 4-OHE(2) increases oxidative stress reducing the level of proteins related to DNA repair. Tocopherols suppressed oxidative stress by scavenging ROS or up-regulating DNA repair elements.
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http://dx.doi.org/10.4162/nrp.2009.3.3.185DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2808717PMC
July 2011

Mammaglobin expression in lymph nodes is an important marker of metastatic breast carcinoma.

Arch Pathol Lab Med 2003 Oct;127(10):1330-4

Department of Pathology, Ajou University School of Medicine, Suwon, Korea.

Context: Organ specificity is a desirable property of a tumor marker, especially in metastatic adenocarcinomas of unknown primary origin. Mammaglobin, a mammary-specific member of the uteroglobin family, is known to be overexpressed in human breast cancer.

Objective: We investigated mammaglobin A expression in metastatic carcinomas of lymph nodes from the breast and various other organs and its usefulness in identifying metastatic carcinoma of the breast. For comparative purposes, we also investigated BRST-1 and BRST-2 expression.

Design: We produced recombinant mammaglobin and polyclonal antimammaglobin antibodies. Mammaglobin expression was analyzed by immunohistochemical staining using a tissue microarray and by reverse transcription-polymerase chain reaction in 210 carcinomas, including those of the breast (n = 70), lung (n = 30), stomach (n = 30), colorectum (n = 25), hepatobiliary tract (n = 20), urinary tract (n = 10), thyroid gland (n = 10), ovary and endometrium (n = 10), and salivary gland (n = 5).

Results: Mammaglobin expression was observed in 59 cases (84.3%) of breast cancer and in 21 cases (15.0%) of nonbreast cancer. The BRST-1 and BRST-2 expression rates were 75.7% and 44.3% in breast cancer and 26.4% and 2.1% in nonbreast cancer, respectively. Mammaglobin is superior to BRST-1 for both specificity and sensitivity and is superior to BRST-2 for sensitivity.

Conclusion: Our data suggest that mammaglobin is one of the first relatively mammary-specific and mammary-sensitive markers. Mammaglobin and BRST-2 appear to represent useful markers for breast cancer and should be used as a component of panels evaluating tumors of unknown primary sites.
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http://dx.doi.org/10.5858/2003-127-1330-MEILNIDOI Listing
October 2003
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