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Yeon-Joo Yook,서영진,Hyoung Jin Kang,Sang-Hyeok Ko,신희영,Jeong Jin Lee,Gajin Jeong,안효섭 대한혈액학회 2010 Blood Research Vol.45 No.3
Background Leukemic cells originate from hypoxic bone marrow, which protects them from anti-cancer drugs. Although many factors that cause drug resistance in leukemic cells have been studied, the effect of hypoxia on drug-induced apoptosis is still poorly understood. Methods In this study, we examined the effect of hypoxia on anti-leukemic drug resistance in leukemic cell lines treated with cobalt chloride (CoCl2), a hypoxia-mimetic agent. Cellular proliferation was evaluated using the methyl thiazolyl tetrazolium (MTT) assay. Flow cytometry analysis and western blots were performed to investigate apoptosis-related proteins. Results Unlike its previously known apoptotic effect, the expression of HIF-1a increased the survival rate of human promyelocytic leukemia HL-60 cells when these cells were exposed to anti-leukemic drugs; these effects were mediated by heat-shock protein HSP70 and the pro-apoptotic protein Bax. Conclusion These findings may provide new insights for understanding the mechanisms underlying hypoxia and for designing new therapeutic strategies for acute myeloid leukemia.
Differential Expression of $PKD2$-Associated Genes in Autosomal Dominant Polycystic Kidney Disease
Yook, Yeon-Joo,Woo, Yu-Mi,Yang, Moon-Hee,Ko, Je-Yeong,Kim, Bo-Hye,Lee, Eun-Ji,Chang, Eun-Sun,Lee, Min-Joo,Lee, Sun-Young,Park, Jong-Hoon Korea Genome Organization 2012 Genomics & informatics Vol.10 No.1
Autosomal dominant polycystic kidney disease (ADPKD) is characterized by formation of multiple fluid-filled cysts that expand over time and destroy renal architecture. The proteins encoded by the $PKD1$ and $PKD2$ genes, mutations in which account for nearly all cases of ADPKD, may help guard against cystogenesis. Previously developed mouse models of $PKD1$ and $PKD2$ demonstrated an embryonic lethal phenotype and massive cyst formation in the kidney, indicating that $PKD1$ and $PKD2$ probably play important roles during normal renal tubular development. However, their precise role in development and the cellular mechanisms of cyst formation induced by $PKD1$ and $PKD2$ mutations are not fully understood. To address this question, we presently created $Pkd2$ knockout and $PKD2$ transgenic mouse embryo fibroblasts. We used a mouse oligonucleotide microarray to identify messenger RNAs whose expression was altered by the overexpression of the $PKD2$ or knockout of the $Pkd2$. The majority of identified mutations was involved in critical biological processes, such as metabolism, transcription, cell adhesion, cell cycle, and signal transduction. Herein, we confirmed differential expressions of several genes including aquaporin-1, according to different $PKD2$ expression levels in ADPKD mouse models, through microarray analysis. These data may be helpful in $PKD2$-related mechanisms of ADPKD pathogenesis.
Mxi1 influences cyst formation in three-dimensional cell culture
( Yeon Joo Yook ),( Kyung Hyun Yoo ),( Seon Ah Song ),( Min Ji Seo ),( Je Yeong Ko ),( Bo Hye Kim ),( Eun Ji Lee ),( Eunsun Chang ),( Yu Mi Woo ),( Jong Hoon Park ) 생화학분자생물학회 2012 BMB Reports Vol.45 No.3
Cyst formation is a major characteristic of ADPKD and is caused by the abnormal proliferation of epithelial cells. Renal cyst formation disrupts renal function and induces diverse complications. The mechanism of cyst formation is unclear. mIMCD-3 cells were established to develop simple epithelial cell cysts in 3-D culture. We confirmed previously that Mxi1 plays a role in cyst formation in Mxi1-deficient mice. Cysts in Mxi1 transfectanted cells were showed by collagen or mebiol gels in 3-D cell culture system. Causative genes of ADPKD were measured by q RT-PCR. Herein, Mxi1 transfectants rarely formed a simple epithelial cyst and induced cell death. Overexpression of Mxi1 resulted in a decrease in the PKD1, PKD2 and c-myc mRNA relating to the pathway of cyst formation. These data indicate that Mxi1 influences cyst formation of mIMCD-3 cells in 3-D culture and that Mxi1 may control the mechanism of renal cyst formation. [BMB reports 2012; 45(3): 189-193]
유지희 ( Ji Hee Yoo ),김주명 ( Joo Myung Kim ),조연진 ( Yeon Jean Cho ),육지형 ( Ji Hyoung Yook ),이희숙 ( Hee Suk Lee ),김미라 ( Mi La Kim ),주관영 ( Kwan Young Joo ) 대한산부인과학회 2009 Obstetrics & Gynecology Science Vol.52 No.6
Objective: The purpose of this study was to describe the clinical presentation and histopathologic findings that help in decisions about management of ovarian mass in childhood and adolescence. Methods: We retrospectively analyzed the data on 307 patients with surgically treated ovarian mass under 20 years of age at the Cheil General Hospital, between January 1995 and December 2005. Results: Of the 307 cases, 40 cases (13%) were ovarian malignancy. The incidence of malignant ovarian tumor increased to 16.9% in 237 neoplastic tumors. Epithelial, germ cell, and sex-cord stromal malignancies accounted for 57.5%, 30% and 12.5%, respectively, of the 40 ovarian malignancies. The stage of the 35 cases (87.5%) with the ovarian malignancy was the FIGO stage I. The incidence of ovarian malignancies increased with larger size, higher CA125 level. Solid ovarian masses on ultrasound were more likely ovarian malignancy. But age and menarchal status was not correlated with ovarian malignancy. Mature cystic teratoma seen in 132 patients (55.7%), was the most common neoplasm of ovary in this age group, and the incidence of bilaterality was 12.1%. On follow up, 4.9% (13/267) of previously diagnosed benign ovarian tumor were reoperated due to recurred or newly developed ovarian tumor. After cystectomy, the recurrence rate of ipsilateral ovarian tumor was 2.8% (4/142). Conclusion: If there is no evidence of malignancy, conservative surgical treatment should be employed to preserve future endocrine function and fertility in this age group.
Yang, Moon-Hee,Yoo, Kyung-Hyun,Yook, Yeon-Joo,Park, Eun-Young,Jeon, Jeong-Ok,Choi, Seo-Hee,Park, So-Young,Woo, Yu-Mi,Lee, Min-Joo,Park, Jong-Hoon Korean Society for Biochemistry and Molecular Biol 2007 Journal of biochemistry and molecular biology Vol.40 No.2
PCD (programmed cell death) is important mechanism for development, homeostasis and disease. To analyze the gene expression pattern in brain cells undergoing PCD in response to serum deprivation, we analyzed the cDNA microarray consisting of 2,300 genes and 7 housekeeping genes of cortical cells derived from mouse embryonic brain. Cortical cells were induced apoptosis by serum deprivation for 8 hours. We identified 69 up-regulated genes and 21 down-regulated genes in apoptotic cells. Based on the cDNA microarray data four genes were selected and analyzed by RT-PCR and northern blotting. To characterize the role of UNC-51-like kinase (ULK2) gene in PCD, we investigated cell death effect by ULK2. And we examined expression of several genes that related with PCD. Especially GAPDH was increased by ULK2. Theses findings indicated that ULK2 is involved in apoptosis through p53 pathway.