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사람 태아 성장세포에서 종양괴사인자 유전자 발현의 조절
류혜명,박주영,최선주,박현숙,고춘명,Ryu, Hye-Myung,Park, Joo-Young,Choi, Sun-Ju,Park, Hyun-Sook,Koh, Choon-Myung 대한미생물학회 2001 Journal of Bacteriology and Virology Vol.31 No.3
Tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) involved in the pathogenesis of multiple sclerosis and contribute to the degeneration of oligodendrocytes as well as neurons. TNF-${\alpha}$ is produced by miocroglia and astrocytes, which also produce hormones and cytokines that influence its biological activity. Astrocytes, the major glial cells in the CNS, are capable of producing TNF-${\alpha}$ at both the mRNA and protein levels in response to interleukine-1 (IL-1) or TNF-${\alpha}$. Two immunosuppressive cytokines, transforming growth factor-${\beta}$ (TGF-${\beta}$) and IL-10, have been shown to influence glial cell function. TGF-${\beta}$ can modulate the activity of glial cells by inhibiting interferon-${\gamma}$ (IFN-${\gamma}$) induced expression of class II major histocompatibility complex (MHC) molecules on astrocytes and microglia. To explore the role of astrocytes in the production of TNF-${\alpha}$, astrocytes were pretreated with IL-10 or TGF-${\beta}$ and then stimulated with IL-1${\beta}$ to determine their effects on TNF-${\alpha}$ production. The secretion of TNF-${\alpha}$ by human fetal astrocytes was markedly inhibited by TGF-${\beta}$ at a low concentration. In contrast IL-10 had no effect on TNF-${\alpha}$ mRNA level. These results show that TGF-${\beta}$ may regulate the expression of TNF-${\alpha}$ in activated human fetal astrocytes.
조지형 ( Ji Hyung Cho ),류혜명 ( Hye Myung Ryu ),진미경 ( Mi Kyung Jin ),전주현 ( Joo Hyun Chun ),현승혜 ( Seung Hyea Hyun ),최지영 ( Ji Young Choi ),허인경 ( In Kyong Hur ),이은영 ( Eun Young Lee ),박선희 ( Sun Hee Park ),김용림 대한신장학회 2008 Kidney Research and Clinical Practice Vol.27 No.4
목적: 염증반응과 섬유화에 관여하는 Transforming growth factor-β1 (TGF-β1)와 이식신에 대한 cytoprotection에 관여하는 vascular endothelial growth factor (VEGF)는 만성 이식신 신병증 (CAN)의 발생과 연관이 있을 것으로 추측되어 왔다. 이에 저자들은 한국인 신이식 수혜자를 대상으로 TGF-β1 및 VEGF 유전자 SNP과 이식신 생존율 및 CAN과의 상관관계에 대해 조사하였다. 방법: 경북대학교병원에서 신이식을 시행한 환자 중 유전자 분석에 동의한 221명과 건강한 대조군 148명을 대상으로 TGF-β1 유전자의 C-509T 및 T869C, VEGF 유전자에 있는 C-2578A, C405G의 유전자형을 분석하였다. 신이식 후 CAN이나 만성 calcineurin inhibitor 신독성으로 진단된 경우를 신병증군 (n=21)으로 그렇지 않은 경우를 정상 이식군 (n=200)으로 분류하였다. 결과: 신이식 환자군과 정상 대조군에서 확인된 TGF-β1 (C-509T, T869C) 및 VEGF 유전자의 SNP (C- 2578A, C405G)의 유전자형의 빈도는 Hardy-Weinberg 평형에 따른 기대빈도와 유의한 차이가 없었고, 신이식 환자군과 정상 대조군에 있어 TGF-β1 및 VEGF 유전자 SNP의 유전자형과 대립형질의 빈도에는 유의한 차이가 없었다. TGF-β1의 C-509T와 T869C 및 VEGF의 C-2578A와 C405G는 강한 유전적 상관 관계를 보였고 (D`=0.78-0.98), 두 군 간 각각의 일배체형 간의 빈도 차이는 없었다. 전체 신이식 환자를 대상으로 TGF-β1 및 VEGF 유전자 SNP의 유전자형에 따라 두 군으로 나누어 Kaplan-Meier 생존분석을 시행한 결과 이식신 생존율은 유의한 차이가 없었고, 저농도 혹은 고농도의 cytokine 생산과 관련된 유전자형에 따른 이식신 생존율도 각 cytokine 모두 유사하였다. 결론: 본 연구에서 조사한 TGF-β1 및 VEGF 유전자 SNP은 한국인 신이식 수혜자에서 이식신 생존 또는 만성 이식신 신병증 발생 여부에 따라 차이를 보이지 않았다. Purpose: Transforming growth factor-β1 (TGF-β1) has been associated with the promotion of renal allograft interstitial fibrosis and thereby chronic allograft nephropathy (CAN). Vascular endothelial growth factor (VEGF) has been shown to contribute to cytoprotection of the graft after kidney transplantation. We investigated the influence of single nucleotide polymorphisms (SNPs) of the TGF-β1 (C-509T and T869C) and the VEGF gene (C-2578A and C405G) on graft survival and the development of CAN. Methods: Genotyping was carried out using a real-time polymerase chain reaction which was performed on the LightCycler480 in 221 Korean renal transplant recipients and 148 healthy controls. According to the presence of CAN or chronic calcineurin inhibitor nephrotoxicity, the recipients were separated into the CAN (n=21) and the No CAN (n=200) groups. Results: The genotype frequencies of the SNPs were in Hardy-Weinberg equilibrium. The distributions of genotypes and alleles did not differ between recipients and controls. No significant differences were observed in the genotype distributions and allele frequencies between the CAN and the No CAN groups. The frequencies of haplotypes were not significantly different between the two groups, either. There were no statistically significant effects of TGF-β1 and VEGF gene polymorphisms on graft survival. Conclusion: This study did not show any statistically significant effects of four selected SNPs of the TGF-β1 and the VEGF genes on the development of CAN and graft survival in Korean renal transplant recipients.
복막투석 환자에서 TGF-β1 유전자 다형성과 동맥경화성 혈관질환 유병율과의 관계
조성 ( Seong Cho ),김찬덕 ( Chan Duck Kim ),류혜명 ( Hye Myung Ryu ),박선희 ( Sun Hee Park ),김용림 ( Yong Lim Kim ) 대한신장학회 2007 Kidney Research and Clinical Practice Vol.26 No.6
Purpose : Atherosclerotic vascular disease (AVD) is a leading cause of morbidity and mortality in patients with end-stage renal disease (ESRD) on peritoneal dialysis (PD). Transforming growth factorbeta1 (TGF-β1) is a multifunctional cytokine that inhibits the atheromatous process. The author studied polymorphisms of the TGF-β1 gene (-509C>T and 869T>C) as genetic susceptibility factors for AVD in PD patients. Methods : Genotyping was carried out using the LightCycler 480 with melting curve analysis function. Prevalent vascular disease was defined by the presence of ischemic heart disease (IHD), peripheral vascular disease (PVD), cerebrovascular disease (CVD), or congestive heart failure (CHF). The presence of AVD was derived by the presence of any vascular disease (i.e., any degree of IHD/PVD/CVD). Results : In total, 109 PD patients were recruited (38.7% male, and 28.7% diabetic). The mean age was 49.1±14.1 years, and mean dialysis duration was 61.3±34.1 months. The most frequent genotype at -509C>T was CT (49.5%) and at 869T>C was TC (47.7%). No significant differences were observed in the genotype distributions of the investigated TGF-β1 (CC:CT:TT, 18.5%:55.6%:25.9%vs 26.8%:47.6%:25.6%, χ2=0.246, p=0.884; TT:TC:CC, 18.5%:55.6%:25.9% vs 28.0%:45.1%:26.8%, χ2=1.188, p=0.552) between AVD group and no AVD group. Conclusion : TGF-β1 gene polymorphisms at both -509C>T and +869T>C were not associated with an increased risk for prevalent vascular diseases. Further studies are required to evaluate the role of TGF-β1 as a candidate gene.