• Clinical and Experimental Reproductive Medicine
• /
• v.34 no.3
• /
• pp.149-157
• /
• 2007

Objective: This study was performed to compare the expression of osteopontin (OPN) mRNA and protein in the eutopic and ectopic endometrial tissues in women with endometriosis and endometrial tissues in women without endometriosis. Methods: A total of 32 women with histologically confirmed endometriosis were recruited for study group. For controls, 34 women undergoing operative treatment for cervical intraepithelial neoplasia (CIN) or benign gynecologic condition other than endometriosis were recruited. At the time of laparoscopy or laparotomy, a biopsy specimen was taken from the endometrial cavity and peritoneal endometrial implant or endometrioma whenever appropriate. We employed real time quantitative RT-PCR to quantify OPN mRNA expression of these tissues and performed western blot analysis to measure the quantity of OPN. Results: The expression of OPN mRNA was significantly higher in both eutopic and ectopic endometrial tissues of women with endometriosis than in endometrial tissues of controls during both proliferative and secretory phase. In the eutopic endometrial tissue of women with endometriosis, OPN mRNA expression significantly increased during the secretory phase compared to the proliferative phase in women with endometriosis as well as controls. However, in the ectopic endometrial tissue, OPN mRNA expression significantly decreased during the secretory phase compared to the proliferative phase. The expression of OPN protein was significantly higher in women with endometriosis than in controls. Conclusion: This study shows the marked expression of OPN mRNA and protein in eutopic and ectopic endometrial tissues in women with endometriosis may be associated with the adhesion and invasion of endometrial explants.

• Journal of dental hygiene science
• /
• v.9 no.4
• /
• pp.427-433
• /
• 2009

Nuclear factor I-C (NFI-C) null mice demonstrated aberrant odontoblast differentiation and abnormal dentin formation. In order to elucidate the mechanisms responsible for these changes, we evaluated the expression of dentin matrix gene after over-expression and inactivation of NFI-C in MDPC-23 cells by reverse transcription-polymerase chain reaction (RT-PCR) analysis. Collagen type I (Col I), osteocalcin (OC), and dentin sialophosphoprotein (DSPP) expression was decreased after inactivation of NFI-C. However, bone sialoprotein (BSP) expression was dramatically increased after inactivation of NFI-C. ALP and DMP4 expression was not changed after inactivation of NFI-C. The expression of alkaline phoshatase (ALP) and dentin matrix protein 4 (DMP4) was increased after over-expression of NFI-C, while Col I, OC, DSPP, and BSP expression was decreased. These findings suggest that odontoblasts after loss of NFI-C lost the phenotype of odontoblasts and acquired those of osteoblasts.

• Tuberculosis and Respiratory Diseases
• /
• v.45 no.4
• /
• pp.760-765
• /
• 1998

Background: Glucose uptake has been found to be increased in cancer cells, and FDG-PET imaging is used for diagnosis of cancer using this phenomenon. However, the exact mechanism of increased glucose uptake in cancer cells has not been clarified. Recent studies demonstrated the presence of glucose transporter(GLUT) mRNA expression in gastrointestinal cancer and head and neck cancer, and suggested that GLUT may be associated with glucose uptake in cancer cells. In lung cancer cells, glucose metabolism is also known to be increased. We evaluated GLUT mRNA expression in human lung cancer cell lines in order to find out the mechanism of increased glucose uptake in lung cancer. Method: Total RNA was isolated from 15 human lung cancer cell lines and immortalized bronchial epithelial cell line(BEAS-2B). After electrophoresis of $20{\mu}g$ total RNA, Northern blot analysis was done using GLUT1 cDNA and GLUT3 cDNA as probes. Results: Thirteen of 14 human lung cancer cell lines expressed GLUT1 mRNA and 10 of 14 human lung cancer cell lines expressed GLUT3 mRNA. Eight human lung cancer cell lines expressed both GLUT mRNAs. BEAS-2B expressed GLUT1 mRNA and did not express detectable GLUT3 mRNA. Conclusion: The increase of glucose metabolism in lung cancer may be associated with GLUT1 and GLUT3 expression.

• Applied Biological Chemistry
• /
• v.44 no.4
• /
• pp.211-214
• /
• 2001

Utilizing the foreign gene expression system of Drosophila melanogaster Schneider line 2(S2) cell, the degree of transient protein and mRNA expression was examined with different terminators. In the case of transient expression, the expression level of green fluorescent protein(GFP) was the highest when the transfection agent was eliminated and then cultivated for 36 to 48 hr. The terminators(SV40 p(A), SV40 small T-antigen and human gastrin 3'UTR) of the expression vector system were each cloned with endostatin; thereafter, the expression levels of the endostatin and its mRNA were compared. When the expression levels of endostatin were compared 36 hr after transfection, the SV40 p(A) terminator showed the highest expression level of endostatin and its mRNA.

• Journal of Yeungnam Medical Science
• /
• v.24 no.1
• /
• pp.67-78
• /
• 2007

Background : Interleukin-18 (IL-18) is one of the principal inducers of interferon-${\gamma}$ (IFN-${\gamma}$) in lymphocytes. Materials and Methods : The effect of IL-18 on the expression of chemokine IP-10(CXCL10) mRNA in C57BL/6 mouse peritoneal macrophages was studied by using Northern blot analysis, enzyme linked immunosobent assay and electrophoretic mobility shift assay. Results : IL-18 was determined to exert no direct effect on the expression of IP-10(CXCL10) mRNA. However, IL-18 pretreatment was determined to play a cooperative role in the synergistic induction of LPS-induced IP-10(CXCL10) mRNA expression. The effect associated with IL-18 pretreatment with regard to the synergistic induction of LPS-induced IP-10 (CXCL10) mRNA expression was detected after 16 hr of IL-18 pretreatment, administered prior to LPS stimulation. The pattern of NF-${\kappa}B$ binding activity during IL-18 pretreatment with LPS stimulation was found to coincide with the expression of IP-10(CXCL10) mRNA. Conclusion : Although IL-18 alone exerts no direct effect on the expression of chemokine IP-10(CXCL10), a definite period of IL-18 pretreatment induces the synergistic expression of LPS-induced IP-10(CXCL10) mRNA. NF-${\kappa}B$ activation is a component of this synergistic effect of IL-18 pretreatment. These results provide useful information, which may facilitate the elucidation of the action mechanisms underlying IL-18 effect on the expression of IP-10(CXCL10) mRNA.

• Journal of Life Science
• /
• v.32 no.3
• /
• pp.222-231
• /
• 2022

This study aimed to confirm the possibility of being used as a cosmetic material material through the verification of the whitening and anti-inflammatory activities of an ethyl acetate fraction from Glechoma hederacea var. longituba (GHEA). The observed electron donating and ABTS⁺ radical scavenging abilities of GHEA were 89.6% and 88.7%, respectively, at 1,000 ㎍/ml concentration, with a tyrosinase inhibitory effect of 22.3% at the same concentration. For cell viability, a rate of 80% or more was observed in all concentrations that treated GHEA on melanoma and macrophage cells. Protein and mRNA expression inhibition was measured by Western blot and RT-PCR for 25, 50, and 100 ㎍/ ml concentrations, and it was confirmed that expression decreases in a concentration-dependent manner as GHEA concentration increases. The inhibition of the whitening-related factors MITF and TRP-2 were superior following GHEA treatment than those of the control group treated with kojic acid of 100 ㎍/ml concentration. For tyrosinase, the lowest mRNA expression rate was 29.1% at 100 ㎍/ml which confirmed excellent inhibition. In analyzing the effects of pro-inflammatory cytokines IL-1β, IL-6, and TNF-α on protein and mRNA expression, IL-6 and TNF-α showed high protein and mRNA inhibition compared to a vitamin C control group. Based on these experimental results, GHEA could be applied as a natural cosmetic material.

• Journal of Life Science
• /
• v.17 no.7 s.87
• /
• pp.976-982
• /
• 2007

The purpose of this study was to determine the modulating effects of histone deacetylase inhibitor, trichostatin A, on the differentiation of mouse C2C12 myoblasts. We demonstrated that trichostatin A induced morphological changes of C2C12 myoblasts into smooth muscles and significantly increased the gene expression of smooth muscle markers including smooth muscle ${\alpha}-actin$ and transgelin. These results were due to the change in the expression level of cell cycle regulators in trichostatin A-treated C2C12 cells. Real-time PCR data revealed that cyclin dependent kinase inhibitor, p21, mRNA expression was significantly increased in trichostatin A-treated C2C12 cells. However, trichostaDn A rapidly decreased cyclin Dl mRNA expression necessary for cell cycle progression in 24hr after treatment. In conclusion, the strong inhibitory effects of trichostatin A on histone deacetylation induced transdifferentiation of C2C12 myoblasts into smooth muscle cells and these results are partly due to the changes in the expression of cell cycle regulators such as p21 and cyclin D1.

• The Journal of the Korea Contents Association
• /
• v.9 no.4
• /
• pp.355-363
• /
• 2009

Increased oxidative stress by abnormal mitochondrial function can damage cell signal transduction and gene expression, and induce insulin resistance or diabetes. Autophagy, however, improve insulin resistance by clearance of malfunctioning mitochondria. Exercise also recovers the muscle dysfunction and degeneration by activating mitochondrial biogenesis. As it seems that exercise and autophagy might act as an orchestrated network to induce mitochondrial biogenesis, we investigated whether autophagy is involved in AMPK signal pathway stimulated by exercise or AICAR to increase mitochondrial biogenesis. And it showed that PGC-1 and mtTFA, but not autophagy marker LC3 mRNA expression were significantly increased by 6 hr of acute exercise. On the other hand, PGC-1 and mtTFA mRNA expression were upregulated by AICAR treatment to C2C12 myotube. However these genes were not inhibited by LC3 siRNA transfection. These results provide the evidence that autopahgy affects on mitochondrial biogenesis through different signal pathway from AMPK signal transduction.

• Development and Reproduction
• /
• v.4 no.1
• /
• pp.61-66
• /
• 2000

This study was investigated to analyze the inactivating point mutation and expression level of follicle-stimulating hormone(FSH) receptor mRNA. In first experiment, we analyzed the point mutation. Peripheral blood was collected from each patient. To screen individuals for the C566T mutation, PCR was performed for exon 7 of the FSH receptor gene in 10 patients. No inactivating point mutation of FSH receptor gene was identified in women with premature ovarian failure. To analyze the expression level of FSH receptor, mRNA expressions were examined by RT-PCR method using specific primers for the FSH receptor. The amount of FSH receptor mRNA expressed in POF patients was lower than that in the control group. But it was not significantly different. These finding suggests that lower expression of FSH receptor in premature ovarian failure patients might be the cause of the low response to the gonadotropin during the hyperstimulation in IVF-ET cycles.

• Journal of Life Science
• /
• v.20 no.1
• /
• pp.103-112
• /
• 2010

Pemetrexed has demonstrated clinical activity in non-small cell lung cancer (NSCLC) as well as other solid tumors. It transports into the cells via reduced folate carrier (RFC) and is polyglutamated by folypolyglutamate synthetase (FPGS). Pemetrexed directly inhibits several folate-dependent enzymes such as thymidylate synthase (TS), dihydrofolate reductase (DHFR), and glycinamide ribonucleotide formyltransferase (GARFT). We investigated the effects of genetic variations and the expression of RFC, FPGS, TS and DHFR enzymes on drug sensitivity to pemetrexed in NSCLC cells. Polymorphisms in RFC, FPGS, and DHFR were genotyped in four NSCLC cells - A549, PC14, HCC-1588, and H226. Real-time RT-PCR and Western blot was performed to evaluate mRNA transcripts and protein of these genes. The cytotoxicity of pemetrexed was measured by SRB assay. In PC14 and H226 cells, increased mRNA expressions of RFC and FPGS were associated with higher cytotoxicity to pemetrexed. 2R/2R genotype of TS and its increased mRNA expression were associated with drug resistance to pemetrexed in A549 cells, whereas 3R/3R genotype in TS with decreased mRNA expression was associated with higher sensitivity in H226 cells. After pemetrexed treatment, an inverse change of DHFR mRNA and protein expression was found. The strongest linkage disequilibrium (LD) was discovered between-1726C>T and -1188A>C SNP of DHFR gene. Our findings suggest the cytotoxic effect of pemetrexed may be associated with genetic polymorphisms and the expression level of genes involved in pemetrexed metabolisms in NSCLC cells.