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게잡이 원숭이에서 Recombinant Human Erythropoietin의 4주간 투여 후 비장 유전자 발현 연구
윤석주(Seokjoo Yoon),황지윤(Ji-Yoon Hwang),임정선(Jung-Sun Lim),정선영(Sun-Young Jeong),김용범(Yong-Bum Kim),김달현(Dal-Hyun Kim),권명상(Myung-Sang Kwon),한상섭(Sang-Seop Han),김충용(Choong-Yong Kim) 한국독성학회 2005 Toxicological Research Vol.21 No.3
We investigated effects of recombinant human erythropoietin (rHuEPO) on profiles of mRNA transcripts in 6 male cynomolgus (M. fascicularis) monkey’s spleen for 4 weeks. Six monkeys, composed of control and treatment group (Control : M1, M2, M3; Treatment : M4, M5, M6) were intravenously administered 3 times per week without or with a dose of rHuEPO 2730 IU/0.1 ㎖/㎏. After 4 weeks rHuEPO treatment, spleen was removed for RNA isolation. Splenic gene expression was assessed using Affymetrix U133A 2.0 arrays containing 18,400 transcripts and variants, including 14,500 well-characterized human genes. Gene expression pattern was very different between individuals even in same treatment. In rHuEPO treated groups showed number of genes were up-or downregulated (M4: 79; M5: 48; M6: 73 genes). Six genes (epidermal growth factor receptor, calgranulin A, estrogen receptor binding site associated antigen, matrix metalloproteinase 19, zinc finger and BTB domain containing 16, progestin and adipoQ receptor) were commonly expressed in rHuEPO treated group. The different individual response could be major considering factor in monkey experiment. Further study is needed to clarify the different individual response to rHuEPO in molecular level. This study will be valuable in the fundamental understanding and validation of molecular toxicology for biogeneric drugs including rHuEPO in cynomolgus monkey.
N-ethyl-N-nitrosourea mutagenesis : 질환모델동물의 개발
조규혁(Kyu-Hyuk Cho),조재우(Jae-Woo Cho),윤석주(Seokjoo Yoon),송창우(Chang-Woo Song) 한국실험동물학회 2004 Laboratory Animal Research Vol.20 No.2
Stepping into the post genome era, geneticists is focusing their studies on gene function and its role in mechanism of human disease. N-ethyl-N-nitrosourea (END) mutagenesis and screening for altered phenotypes have been used effectively in many model mice to identify mutation in genes that control biological processes. ENU is currently one of the most powerful mutagen for the production of mutant in mice. This review includes 1) the principle of mutation by ENU treatment, 2) the process of mutagenesis, 3) screening of phenotypes, 4) mating methods of phenodeviants, breeding methods of high technology and cryopreservation, 5) result of the inside and outside of the country mutant mice development, 6) mapping and mutation analysis of cause genes, and 7) prospect in the future.
ENU 돌연변이 유발법에 의한 소안구증 및 각막혼탁을 보이는 유전성 마우스 계통 확립
조재우(Jae-Woo Cho),조규혁(Kyu-Hyuk Cho),윤석주(Seokjoo Yoon),송창우(Chang-Woo Song) 한국실험동물학회 2004 Laboratory Animal Research Vol.20 No.4
본 연구를 통해 개발된 소안구증 및 각막 혼탁 마우스는 교배 실험을 통해 유전성을 확인할 수 있었고 상염색체성 우성 열성 방식을 나타내었다. 눈이 발생하지 않거나 소안구증을 나타내는 개체의 경우 눈의 발생 흔적이라고 할 수 있는 까만 점이 출생 시 보이지 않거나 작았고 그렇지 않은 경우 눈꺼풀이 열리고 이유할 시점에 관찰할 때 눈에 혼탁을 볼 수 있었다. 조직학적 검사 결과 안구 전체적인 기형 소견이 관찰되었다. 렌즈 뿐만 아니라 각막 및 망막층의 이상, 홍채의 기형, 렌즈에 색소층의 유착 등이 특징이었다. 인간에 있어서도 유사한 질환이 보고되어 있고 맹안과도 관계가 있어 본 연구를 통해 개발된 돌연변이 마우스는 인간의 소안구증 및 각막이상과 관련된 질환의 병인을 분석하는데 사용될 수 있는 모델로써 유용할 것으로 사료된다. ENU(N-ethyl-N-nitrosourea)has known as the most efficient chemical mutagen in the germ cell than any other chemicals. Male C57BL/6 was injected 200 ㎎/㎏ ENU. Through mating between treated male and normal female mouse of the same strain, eye abnormal offspring is produced in the next generation. The mutants show eye dysmorphology in one or both sides. It has small and opaque eyes and frequently anophthalmia. It is usually distinguishable from normal mouse at 2 weeks of age. In the gross observation, it exhibits complex phenotypes like irregular pupil, corneal opacity, smaller and irregular lens morphology. Histologically, there are absent or abnormal iris and irregular retinal layer. The part of pigment layer often adheres to posterior lens. The mutant mouse is viable. In the mating between normal & heterozygous mice, 52% mutants are generated and its sex ratio is 1:1. Therefore, it supposes that mutation gene transfer to the next generation by autosomal dominant mode. Compared inheritance mode and phenotypes of this mutant with other reported similar mice, Pax6 gene may be a candidate of this causative gene.