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Ha Young‐Ran,Jeong Se‐Jin,Jang Chang‐Won,Chang Kyu‐Sik,Kim Hyun‐Woo,Cho Shin‐Hyoung,Lee Hee‐Il 한국곤충학회 2021 Entomological Research Vol.51 No.2
Mosquitoes have adapted to various environmental conditions. Symbionts with mosquitoes impact this adaptation in different environments. In the field, mosquitoes could get exposed to antibiotics during their developmental period, which could reduce or eliminate their symbiotic microbes. However, the side effects of the antibiotics on the ovary and reproductive physiology of the Asian tiger mosquito, Aedes albopictus remains unknown. In this study, we investigated the effects of tetracycline and combinations of rifampicin and tetracycline at environmentally acceptable levels on the reproductive physiology of ovaries in Ae. albopictus. Rifampicin and tetracycline in combination reduced the hatching rate and fertility of Ae. albopictus compared to the untreated control group. These antibiotics induced histopathological damage and reactive oxygen species production in the ovaries. The combination of antibiotics decreased the expression of surface protein of Wolbachia (WSP) in Ae. albopictus. Additionally, the expression of Toll like receptor 2 (TLR2) and Myd88 were triggered by the combinations. The findings demonstrate the detrimental effects of antibiotics, particularly combinations of rifampicin and tetracycline, on the reproductive capacity of Ae. albopictus females.
Jang, Jae-Woo,Song, Yeonhwa,Kim, Se-Hyuk,Kim, Jin-sun,Kim, Kang mo,Choi, Eun Kyung,Kim, Joon,Seo, Haeng Ran Elsevier 2017 Cancer letters Vol.389 No.-
<P><B>Abstract</B></P> <P>Hepatocellular carcinoma (HCC) is the seventh most common malignant tumor and the third leading cause of cancer-related death in the world. Cancer stem cells (CSCs) are small subpopulation of cells within tumors that drive chemoresistance and tumor recurrence in various cancers. We characterized CSCs in primary HCC and identified CD133 as a CSC surface marker. CD133<SUP>+</SUP> HCC cells displayed more stem cell-like properties, tumor spheroid-forming ability, chemoresistance, migration ability, and tumorigenic capacity than CD133<SUP>-</SUP> HCC cells. The biological function and molecular mechanism of CD133 remain unclear. HCC cell lines with a high level of CD133 expression overexpressed EGFR, which is overexpressed in approximately 70% of conventional HCCs. CD133 depletion destabilized EGFR by augmenting EGFR internalization and thus inhibited EGFR-AKT signaling. CD133 would therefore serve to sustain aberrant EGFR-mediated oncogenic signaling. Furthermore, EGFR-deficient CD133<SUP>+</SUP> HCC cells manifested greater sensitivity to anticancer drugs and less spheroid-formation capacity than control CD133<SUP>+</SUP> HCC cells. Our results strongly indicate that CD133 facilitates CSC-like properties by stabilizing EGFR-AKT signaling in HCC. It might therefore be feasible to use CD133 as a novel target to sensitize HCC cells that manifest resistance to EGFR-targeted therapy.</P> <P><B>Highlights</B></P> <P> <UL> <LI> CD133, a CSC marker is identified in primary HCCs and HCC cell lines. </LI> <LI> The expression of EGFR is correlated with The expression of CD133 in HCC cells. </LI> <LI> CD133 induces CSCs properties through the EGFR stabilization. </LI> <LI> The stabilization of EGFR by CD133 activates EGFR-AKT signaling in HCCs. </LI> <LI> CD133 might be a novel target to sensitize HCC cells that manifest resistance to EGFR-targeted therapy. </LI> </UL> </P>
Jang, Soojin,Ryu, Se Min,Lee, Jooyeon,Lee, Hanbyeol,Hong, Seok-Ho,Ha, Kwon-Soo,Park, Won Sun,Han, Eun-Taek,Yang, Se-Ran The Korean Academy of Tuberculosis and Respiratory 2019 Tuberculosis and Respiratory Diseases Vol.82 No.2
Background: Idiopathic pulmonary fibrosis involves irreversible alveolar destruction. Although alveolar epithelial type II cells are key functional participants within the lung parenchyma, how epithelial cells are affected upon bleomycin (BLM) exposure remains unknown. In this study, we determined whether BLM could induce cell cycle arrest via regulation of Schlafen (SLFN) family genes, a group of cell cycle regulators known to mediate growth-inhibitory responses and apoptosis in alveolar epithelial type II cells. Methods: Mouse AE II cell line MLE-12 were exposed to $1-10{\mu}g/mL$ BLM and $0.01-100{\mu}M$ baicalein (Bai), a G1/G2 cell cycle inhibitor, for 24 hours. Cell viability and levels of pro-inflammatory cytokines were analyzed by MTT and enzyme-linked immunosorbent assay, respectively. Apoptosis-related gene expression was evaluated by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR). Cellular morphology was determined after DAPI and Hoechst 33258 staining. To verify cell cycle arrest, propidium iodide (PI) staining was performed for MLE-12 after exposure to BLM. Results: BLM decreased the proliferation of MLE-12 cells. However, it significantly increased expression levels of interleukin 6, tumor necrosis factor ${\alpha}$, and transforming growth factor ${\beta}1$. Based on Hoechst 33258 staining, BLM induced condensation of nuclear and fragmentation. Based on DAPI and PI staining, BLM significantly increased the size of nuclei and induced G2/M phase cell cycle arrest. Results of qRT-PCR analysis revealed that BLM increased mRNA levels of BAX but decreased those of Bcl2. In addition, BLM/Bai increased mRNA levels of p53, p21, SLFN1, 2, 4 of Schlafen family. Conclusion: BLM exposure affects pulmonary epithelial type II cells, resulting in decreased proliferation possibly through apoptotic and cell cycle arrest associated signaling.
Se-Ran Yang,Soojin Jang,Jooyeon Lee,Se Min Ryu,Hanbyeol Lee,Jeong-Ran Park,Aera Jang,Dongwook Kim,Hyejin Kim 한국예방수의학회(구 한국수의공중보건학회) 2017 예방수의학회지 Vol.42 No.2
Colorectal cancer is a major cause of morbidity and mortality that accounts for over 9% of all incidences of cancer. Additionally, colorectal cancer is widely recognized as an environmental disease related to ill-defined cultural, social and lifestyle factors including physical activity, obesity, cigarette smoking and heavy alcohol consumption. Accordingly, natural phytochemicals and extracts have attracted attention because of their beneficial biological effects. Coenzyme Q10 (CoQ10) is a common supplementary medicine applied to increase bioenergetic capacity in various diseases. Therefore, in this study, we investigated whether CoQ10 treatment has any inhibitory effects and its related cellular mechanisms in human colon cancer HCT116 cells. A MTT assay revealed that CoQ10 slightly decreased the proliferation of HCT116 cells; however, glutathione- and superoxide dismutase- activity were unchanged in response to CoQ10 treatment. A DCF-DA assay revealed that CoQ10 slightly increased ROS release of HCT116 cells. However, in a nitric oxide (NO) assay, CoQ10 significantly increased NO production in a dose-dependent manner. The results of western blot analysis revealed that the protein levels of Bax, p21 and p53 were increased, whereas the protein level of Bcl2 was decreased suggesting that the CoQ10-mediated inhibitory mechanism is associated with apoptotic signaling. Taken together, our findings indicate that CoQ10 has an inhibitory effect on the growth of colon cancer cells via NO production that is associated with regulation of factors involved in apoptotic signaling including Bax, Bcl2, p21 and p53.
Se Jin Jeong,Chang won Jang,Jin Hwan Jeon,Gi-Hun Kim,E-Hyun Shin,Young-Ran Ju,Kyu-Sik Chang 한국응용곤충학회 2016 한국응용곤충학회 학술대회논문집 Vol.2016 No.10
Control of the vector mosquitoes is critical for implementation of patient’s decrease. Vector mosquito control has been mainly carried out using pesticides in Republic of Korea (ROK), which has developed the resistance against selected insecticides. Voltage-gated sodium channel (VGSC) and Acethylcholine esterase (AchE) are the target of several classes of insecticides. Genetic mutations of VGSC and AchE have been documented to confer resistances to pyrethroids and organophosphates in mosquitoes, respectively. In our studies, the insecticidal resistable level of An. sinensis from four malaria risk areas near Demilitarized Zone (DMZ) was measured. The partial sequence of An. sinensis voltage gated sodium channel (VGSC) IIS6 domain for Kdr gene and ace1 gene for AchE was sequenced. An. sinensis from two areas demonstrated significantly higher resistance to pyrethroids and mutation rates of Kdr gene were comparatively higher. In all tested areas An. sinensis showed high insecticidal resistance to organophosphates and > 70% of mutation rates of ace1 gene ware higher. Understanding the mechanisms of insecticide resistance among vector mosquitoes populations is very important to efficient and effective vector control.
Pyrethroid resistance of Anopheles sinensis from two malaria occurrence areas in ROK, 2016
Se-Jin Jeong,Chang won Jang,Young-Ran Ju,Kyu-Sik Chang 한국응용곤충학회 2017 한국응용곤충학회 학술대회논문집 Vol.2017 No.04
Anopheles sinensis is an important vector for Plasmodium vivax and thus has been targeted with pyrethroids in Republic of Korea. Using the direct contact mortality bioassay, two field populations of An. sinensis from Ganghwa-gun and Goyang-si were characterized for their resistance to pyrethroids with RR ratio values (Resistant ratio to imidacloprid) of 125.6 to 203.8 folds and 80.0 to 120 folds, respectively. Genomic DNA was used for Allele-specific PCR (AS-PCR) genotyping of the sodium channel genes to detect L1014S mutations. The homozygous susceptible Leu/Leu genotype in Ganghwa-gun and Goyang-si was 5.0% and 11.3% and the resistance genotypes were 95.0% and 88.7%, respectively. The homozygous Phe/Phe resistance genotype was the most prevalent as 35.4% in Ganghwa-gun and 44.0% in Goyang-si. Hence, this study suggests that malaria vector control programs should be prepared for the management of pyrethroid insecticide resistance.
Study of fibroblast growth factor 2 administration in bleomycin induced pulmonary fibrosis mice
Se Bi Lee,Hyeokku Lee,Jungyu Baek,Eunhyeok Choi,Hyunseung Lee,Juhyeok Hong,Jaehyun Kim,Jeong Yun Park,Gichang Jeong,Jieun Jeon,Jooyeon Lee,Jaehyun Park,Jimin Jang,Sang-Ryul Cha,Se-Ran Yang 한국실험동물학회 2023 한국실험동물학회 학술발표대회 논문집 Vol.2023 No.2