• 제목/요약/키워드: Migration factor

검색결과 569건 처리시간 0.027초

Macrophage Migration Inhibitory Factor (MIF) Interacts with Bim and Inhibits Bim-mediated Apoptosis

  • Liu, Lingfeng;Chen, Jinzhong;Ji, Chaoneng;Zhang, Jiayi;Sun, Junlei;Li, Yao;Xie, Yi;Gu, Shaohua;Mao, Yumin
    • Molecules and Cells
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    • 제26권2호
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    • pp.193-199
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    • 2008
  • The pro-apoptotic Bcl-2 family member Bim acts as a sensor for apoptotic stimuli and initiates apoptosis through the mitochondrial pathway. To identify novel regulators of Bim, we employed the yeast two-hybrid system and isolated the human gene encoding macrophage migration inhibitory factor (MIF), a ubiquitously expressed proinflammatory mediator that has also been implicated in cell proliferation, the cell cycle and carcinogenesis. The interaction between MIF and Bim was confirmed by both in vitro and in vivo protein interaction assays. Intriguingly, protein complexes between MIF and the three major Bim isoforms (BimEL/BimL/BimS) could be detected in HEK293 and K562 cells, especially in cells undergoing apoptosis. Moreover, exogenous expression of MIF partially inhibited Bim-induced apoptosis in HEK293 cells. SiRNA-mediated knockdown of MIF increased apoptosis in K562 cells exposed to the chemical oxidant diamide. Endogenous MIF may regulate the pro-apoptotic activity of Bim and inhibit the release of cytochrome c from mitochondria.

Polymorphism in Macrophage Migration Inhibitory Factor -173GC in Pediatric Patients with Autoimmune Hepatitis

  • Alsayed, Mona Abdel Latif;Elbeah, Shymaa Mohsen;El-Desoky, Manal M.;Elziny, Shereen Magdy;Megahed, Ahmed
    • Pediatric Gastroenterology, Hepatology & Nutrition
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    • 제23권1호
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    • pp.63-71
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    • 2020
  • Purpose: Autoimmune hepatitis (AIH) is a chronic disease that may lead to cirrhosis. The immunopathogenesis of AIH is not fully understood and it mainly involves T-cell mediated mechanism. Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine that promotes T cell response and its polymorphism may serve as a severity marker of AIH. No previous study has considered investigating MIF polymorphism in children with AIH. Methods: Forty-two children with definite diagnosis of AIH were enrolled along with 100 age and sex matched controls. All participants were tested for polymorphism at -173GC (rs755622) of MIF gene. All patients received the standard protocol of steroid plus azathioprine to achieve remission. Liver biopsy was performed at time of diagnosis for all patients and only 18 of them underwent a second biopsy after treatment. Results: No statistically significant differences in the frequency of the genotypes GG and GC or in allele distribution were found in both patient and control groups (p=0.590, 0.640 respectively). Initial alanine aminotransferase (ALT) levels at the time of presentation was significantly higher in the GC group than GG group (p=0.020). GC genotype significantly correlated with disease relapse (r=0.41, p=0.007). Regression of necroinflammation and the fibrosis score in the second liver biopsy was statistically significant in the GG group (p<0.0001, p=0.010 respectively). Conclusion: MIF -173GC polymorphism is associated with clinically significant markers of pediatric AIH, including increased initial serum ALT levels, may help predict necroinflammatory/fibrosis regression effectively, following immunosuppressive treatment.

자궁내막종의 감별진단을 위한 난소낭종 환자의 혈청 Macrophage Migration Inhibitory Factor (MIF) 농도의 진단적 유용성에 대한 연구 (Macrophage Migration Inhibitory Factor (MIF) Concentration in the Serum of Patients with Ovarian Cysts for Differential Diagnosis of Endometrioma)

  • 김만기;김유래;홍승화;박연진;지일운;정은환;김학순
    • Clinical and Experimental Reproductive Medicine
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    • 제32권3호
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    • pp.287-293
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    • 2005
  • Objective: To evaluate the usefulness of serum concentrations of macrophage migration inhibitory factor (MIF) of patients with ovarian cysts for differential diagnosis of endometrioama. Method: From Jan. 2003 to Dec. 2004, preoperative serum MIF levels were assessed in 28 women with endometrioma, 32 with benign epithelial tumor, 23 with functional and simple cysts, 22 with benign mature cystic teratoma, and 25 women without ovarian tumor as control. MIF levels were determined using an ELISA (Quantikine Human MIF immunoassay, R&D Systems, Inc., USA). Results: Mean MIF levels were higher in all groups with benign tumors than control (all p<0.01), but there was no significant difference between benign tumor groups (p=0.95). There was no significant correlation between MIF levels and tumor volume, body mass index (BMI) (p=0.635, 0.674 respectively) Serum MIF level had significant correlation with count of WBC and neutrophils (p=0.008, 0.024 respectively), but had no correlation with count of lymhocytes and monocytes (p=0.688, 0.294 respectively). Conclusions: This study showed a marked increase in MIF concentrations in the peripheral blood of patients with endometrioma, but there was no significant difference with other benign tumors. Serum MIF level had significant correlation with count of WBC and neutrophils. These suggest serum MIF level has no usefulness for differential diagnosis of endometrioma from other benign ovarian cysts.

ROLES OF MAPK PATHWAYS IN GDNF-INDUCED GLIOMA CELL MIGRATION

  • Hyun Song;Chung, Dong-June;Choung, Pill-Hoon;Aree Moon
    • 한국독성학회:학술대회논문집
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    • 한국독성학회 2002년도 Molecular and Cellular Response to Toxic Substances
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    • pp.140-140
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    • 2002
  • Glial cell-derived neurotrophic factor (GDNF) is a potent neurotrophic factor that enhances survival of midbrain doparminergic neuron and is a member of the transforming growth factor-b superfamily. GDNF and its receptors are widely distributed in brain and are believed to be involved in the control of neuron survival, proliferation and differentiation.(omitted)

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결혼이주여성의 결혼적응에 관한 연구 (A Study on the Marital Adjustment Among Marriage Migration Females)

  • 김현숙
    • 한국사회복지학
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    • 제62권2호
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    • pp.135-159
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    • 2010
  • 본 연구는 결혼이주여성의 결혼적응에 영향을 미치는 요인을 파악하고자 하였다. 분석에 활용한 자료는 부산대학교 사회과학연구소가 조사한 "결혼이주여성의 자아탄력성과 결혼적응"이다. 분석은 각 독립변수와 결혼적응의 관계를 다변량분석과 중다회귀분석을 통해 살펴보았다. 연구결과에 의하면, 결혼만족은 배우자지지, 가족생활스트레스, 의사소통수준이 영향을 미치는 것으로 나타났다. 이혼 의도는 자녀수, 가족생활스트레스가 영향을 미치는 것으로 나타났다. 부부간 애정은 결혼기간, 배우자 지지, 의사소통수준이 영향을 미치는 것으로 나타났다. 결혼이주여성의 결혼적응에서 가족생활스트레스가 공통적이며, 가장 영향력이 큰 변수로 나타났다. 결혼이주여성들의 가족생활스트레스를 줄이기 위한 체계적이고 구조적인 지원이 필요하다는 것을 제안하였다.

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Pitavastatin Regulates Ang II Induced Proliferation and Migration via IGFBP-5 in VSMC

  • Ha, Yu Mi;Nam, Ju-Ock;Kang, Young Jin
    • The Korean Journal of Physiology and Pharmacology
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    • 제19권6호
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    • pp.499-506
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    • 2015
  • Angiotensin II (Ang II), a key mediator of hypertensive, causes structural changes in the arteries (vascular remodeling), which involve alterations in cell growth, vascular smooth muscle cell (VSMC) hypertrophy. Ang II promotes fibrotic factor like IGFBP5, which mediates the profibrotic effects of Ang II in the heart and kidneys, lung and so on. The purpose of this study was to identify the signaling pathway of IGFBP5 on cell proliferation and migration of Ang II-stimulated VSMC. We have been interested in Ang II-induced IGFBP5 and were curious to determine whether a Pitavastatin would ameliorate the effects. Herein, we investigated the question of whether Ang II induced the levels of IGFBP5 protein followed by proliferation and migration in VSMC. Pretreatment with the specific Angiotensin receptor type 1 (AT1) inhibitor (Losartan), Angiotensin receptor type 2 (AT2) inhibitor (PD123319), MAPK inhibitor (U0126), ERK1/2 inhibitor (PD98059), P38 inhibitor (SB600125) and PI3K inhibitor (LY294002) resulted in significantly inhibited IGFBP5 production, proliferation, and migration in Ang II-stimulated VSMC. In addition, IGFBP5 knockdown resulted in modulation of Ang II induced proliferation and migration via IGFBP5 induction. In addition, Pitavastatin modulated Ang II induced proliferation and migration in VSMC. Taken together, our results indicated that Ang II induces IGFBP5 through AT1, ERK1/2, P38, and PI3K signaling pathways, which were inhibited by Pitavastatin. These findings may suggest that Pitavastatin has an effect on vascular disease including hypertension.

이동 에이전트의 최적 이주 비용을 위한 플랫폼 설계 (Platform Design for Optimal Migration Cost of Mobile Agents)

  • 김완성;복경수;신재룡;유재수
    • 한국정보통신학회논문지
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    • 제8권1호
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    • pp.137-149
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    • 2004
  • 네트워크의 발달과 다양한 서비스의 요구에 따라 새로운 소프트웨어의 패러다임에 대한 요구가 증가되고 있다. 이와 함께 이동 에이전트에 대한 많은 연구가 진행 중이다. 이동 에이전트의 수행에 있어 이주비용은 이동 에이전트의 성능에 많은 영향을 미친다. 본 논문에서 이동에이전트의 이주비용을 최적화하기 위한 기법을 제안한다. 제안하는 이주기법의 특징은 다음과 같다. 첫째, 네트워크 상태 및 플랫폼 상태변화에 적절하게 대응할 수 있는 동적 경로를 생성하여 에이전트 수행 효율을 높인다. 둘째, 수행할 코드를 프리패칭하여 이동 데이터 양을 줄이고, 필요한 에이전트를 미리 인스턴스시켜 수행 시간을 단축한다. 셋째, 체크포인트 기법을 사용하여 에이전트 수행 중에 에러가 발생할지라도 에이전트는 재 수행을 하지 않고 에러 이전의 상태로 복구하는 방법을 사용하여 수행 효율을 높인다. 또한, 시뮬레이션을 통해 기존방법과 제안하는 방법을 비교 평가한다. 시뮬레이션 결과분석을 통해 이주관점에서 제안한 방법들이 기존방법들에 비해 성능이 매우 향상됨을 보인다.

TATA-Binding Protein-Related Factor 2 Is Localized in the Cytoplasm of Mammalian Cells and Much of It Migrates to the Nucleus in Response to Genotoxic Agents

  • Park, Kyoung-ae;Tanaka, Yuji;Suenaga, Yusuke;Tamura, Taka-aki
    • Molecules and Cells
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    • 제22권2호
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    • pp.203-209
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    • 2006
  • TBP (TATA-binding protein)-related factor 2 (TRF2) regulates transcription during a nuber of cellular processes. We previously demonstrated that it is localized in the cytoplasm and is translocated to the nucleus by DNA-damaging agents. However, the cytoplasmic localization of TRF2 is controversial. In this study, we reconfirmed its cytoplasmic localization in various ways and examined its nuclear migration. Stresses such as heat shock, redox agents, heavy metals, and osmotic shock did not affect localization whereas genotoxins such as methyl methanesulfonate (MMS), cisplatin, etoposide, and hydroxyurea caused it to migrate to the nucleus. Adriamycin, mitomycin C and ${\gamma}$-rays had no obvious effect. We determined optimal conditions for the nuclear migration. The proportions of cells with nuclei enriched for TRF2 were 25-60% and 5-10% for stressed cells and control cells, respectively. Nuclear translocation was observed after 1 h, 4 h and 12 h for cisplatin, etoposide and MMS and hydroxyurea, respectively. The association of TRF2 with the chromatin and promoter region of the proliferating cell nuclear antigen (PCNA) gene, a putative target of TRF2, was increased by MMS treatment. Thus TRF2 may be involved in genotoxin-induced transcriptional regulation.

환원환경에서 암반 균열을 통한 우라늄 이동 및 지연 특성 (Migration and Retardation Properties of Uranium through a Rock Fracture in a Reducing Environment)

  • 백민훈;박정균;조원진
    • 방사성폐기물학회지
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    • 제5권2호
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    • pp.113-122
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    • 2007
  • 본 연구에서는 타당한 지하조건을 모사하기 위한 실험장치를 글로버박스(Glove-box) 내에 설치하고 천연지하수 및 자연균열을 가진 화강암 시추코어를 이용하여 핵종이동 실험을 수행하였다. 암반코어의 균열을 통한 지하수 유동을 해석하기 위하여 비수착성 음이온 핵종인 Br로 지하수 유동실험을 수행하였다. 암반 균열을 통한 우라늄 이동 실험결과에서 유출된 우라늄의 파과곡선이 비수착성 핵종인 Br와 유사한 거동을 보여주었는데, 이는 주어진 지하수 조건에서 우라늄이 주로 탄산염과 결합된 음이온 복합체로 이동하기 때문인 것으로 추정된다. 아울러 균열충전광물에 대한 우라늄의 회분식 수착실험을 수행한 결과, 균열충전광물에 대한 우라늄의 분배계수 $K_d$는 약 2.7 mL/g로 낮게 나타났다. 이러한 우라늄 수착실험 결과는 빠른 유출을 보인 우라늄 이동실험 결과와 일치한다. 균열암반을 통한 우라늄 이동의 지 연 특성을 보다 자세히 분석하기 위하여 회분식 수착실험으로 부터 구한 $K_d$값을 이용해 지연인자 $R_d$$({\sim}16.2)$를 구하고 이동실험 결과로부터 구한 $R_d$$({\sim}14.3)$과 비교한 결과, 서로 매우 유사한 지연인자 값을 가진다는 것을 알 수 있었다. 이는 화강암 코어의 균열을 통한 우라늄의 이동 지연이 주로 균열충전광물에 의해 이루어지고 있음을 의미하는 것이라고 하겠다.

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Effects of Down-regulation of HDAC6 Expression on Proliferation, Cell Cycling and Migration of Esophageal Squamous Cell Carcinoma Cells and Related Molecular Mechanisms

  • Li, Ning;Tie, Xiao-Jing;Liu, Pei-Jie;Zhang, Yan;Ren, Hong-Zheng;Gao, Xin;Xu, Zhi-Qiao
    • Asian Pacific Journal of Cancer Prevention
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    • 제14권2호
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    • pp.685-689
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    • 2013
  • Objective: To study the effects of down-regulation of HDAC6 expression on proliferation, cell cycling and migration of esophageal squamous cell carcinoma (ESCC) cells and related molecular mechanisms. Methods: ESCC cell line EC9706 cells were randomly divided into untreated (with no transfection), control siRNA (transfected with control siRNA) and HDAC6 siRNA (transfected with HDAC6 small interfering RNA) groups. Effects of HDAC6 siRNA interference on expression of HDAC6 mRNA and protein in EC9706 cells were investigated by semi-quantitative RT-PCR, Western blotting and immunocytochemistry methods. Effects of down-regulation of HDAC6 expression on cell proliferation, cell cycle, and cell migration were studied using a CCK-8 kit, flow cytometry and Boyden chambers, respectively. Changes of mRNA and protein expression levels of cell cycle related factor (p21) and cell migration related factor (E-cadherin) were investigated by semi-quantitative RT-PCR and Western blotting methods. Results: After transfection of HDAC6 siRNA, the expression of HDAC6 mRNA and protein in EC9706 cells was significantly downregulated. In the HDAC6 siRNA group, cell proliferation was markedly inhibited, the percentage of cells in G0/G1 phase evidently increased and the percentage of cells in S phase decreased, and the number of migrating cells significantly and obviously decreased. The mRNA and protein expression levels of p21 and E-cadherin in the HDAC6 siRNA group were significantly higher than those in the untreated group and the control siRNA group, respectively. Conclusions: HDAC6 siRNA can effectively downregulate the expression of HDAC6 mRNA and protein in EC9706 cells. Down-regulation of HDAC6 expression can obviously inhibit cell proliferation, arrest cell cycling in the G0/G1 phase and reduce cell migration. The latter two functions may be closely related with the elevation of mRNA and protein expression of p21 and E-cadherin.