• Title, Summary, Keyword: TNF-${\alpha}$

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Regulation of Preimplantation Development of Mouse Embryos by Insulin and Tumor Necrosis Factor alpha (생쥐 초기배아에서 Insulin과 Tumor Necrosis Factor $\alpha$에 의한 발생의 조절)

  • 계명찬;한현주;최진국
    • Development and Reproduction
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    • v.5 no.2
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    • pp.101-106
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    • 2001
  • Present study was aimed to verify the role of insulin and TNF-$\alpha$ in development of preimplantation embryos. Mouse morula were cultured for 40 hr in the presence or absence of insulin(400 ng/ml) and TNF-$\alpha$ (50 ng/ml). The morphological development, cell number of blastomeres per blastocyst, and mitogen activated protein kinase(MAPK) activity were examined. The developmental rate and cell number per embryo were the highest in insulin treatment group and the lowest in TNF-$\alpha$ treatment group. There was no significant difference in developmental rate between control and insulin plus TNF-$\alpha$ group. Taken together, it suggested that TNF-$\alpha$ impaired embryonic development and that insulin rescued developmental impairment imposed by TNF-$\alpha$. In blastocysts, insulin treatment significantly increased MAPK activity. TNF-$\alpha$ decreased the MAPK activity in a concentration-dependent manner. In the TNF-$\alpha$(50 ng/ml) -primed embryos, activation of MAPK by insulin was attenuated. In conclusion, these results suggest that there was a cross talk between insulin and TNF-$\alpha$ by means of activation of MAPK in preimplantation embryos and that insulin might rescue damage of embryos exposed to TNF-$\alpha$.

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TNF-α in the Pleural Fluid for the Differential Diagnosis of Tuberculous and Malignant Effusion (결핵성 및 악성흉수의 감별에 있어 흉수 내 TNF-α의 유용성)

  • Kim, Hye Jin;Shin, Kyeong Cheol;Lee, Jae Woong;Kim, Kyu Jin;Hong, Yeong Hoon;Chung, Jin Hong;Lee, Kwan Ho
    • Tuberculosis and Respiratory Diseases
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    • v.59 no.6
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    • pp.625-630
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    • 2005
  • Background : Determining the cause of an exudative pleural effusion is sometimes quite difficult, especially between malignant and tuberculous effusions. Twenty percent of effusions remain undiagnosed even after a complete diagnostic evaluation, including pleural biopsy. The activity of tumor necrosis factor-alpha (TNF-${\alpha}$), which is the one of proinflammatory cytokines, is increased in both infectious and malignant effusions. The aim of this study was to investigate the diagnostic efficiency of TNF-${\alpha}$ activity in distinguishing tuberculous from malignant effusions. Methods : 46 patients (13 with malignant pleural effusion, 33 with tuberculous pleural effusion) with exudative pleurisy were included. TNF-${\alpha}$ concentrations were measured in the pleural fluid and serum samples using an enzyme-linked immunosorbent assay (ELISA). In addition, TNF-${\alpha}$ ratio (pleural fluid TNF-${\alpha}$ : serum TNF-${\alpha}$) was calculated. Results : TNF-${\alpha}$ concentration and TNF-${\alpha}$ ratio in the pleural fluid were significantly higher in the tuberculous effusions than in the malignant effusions (p<0.05). However, the serum levels of TNF-${\alpha}$ in the malignant and tuberculous pleural effusions were similar (p>0.05). The cut off points for the pleural fluid TNF-${\alpha}$ level and TNF-${\alpha}$ ratio were found to be 136.4 pg/mL and 6.4, respectively. The sensitivity, specificity and area under the curve were 81%, 80% and 0.82 for the pleural fluid TNF-${\alpha}$ level (p<0.005) and 76%, 70% and 0.72 for the TNF-${\alpha}$ ratio (p<0.05). Conclusion : We conclude that pleural fluid TNF-${\alpha}$ level and TNF-${\alpha}$ ratio can distinguish a malignant pleural effusion from a tuberculous effusion, and can be additional markers in a differential diagnosis of tuberculous and malignant pleural effusion. The level of TNF-${\alpha}$ in the pleural fluid could be a more efficient marker than the TNF-${\alpha}$ ratio.

The Ability of Anti-$TNF-{\alpha}$ Antibodies Produced in Sheep Colostrums

  • Yun, Sung-Seob
    • Journal of Dairy Science and Biotechnology
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    • v.25 no.2
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    • pp.1-4
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    • 2007
  • The present study was performed to elucidate the ability of anti-$TNF-{\alpha}$ antibodies produced in sheep colostrums to neutralise $TNF-{\alpha}$ action in a cell-based bioassay and in a small animal model of intestinal inflammation. Colostrums from sheep immunized against $TNF-{\alpha}$ significantly inhibited $TNF-{\alpha}$ bioactivity in the cell based assay. The higher than anticipated variability in the two animal models precluded assessment of the ability of antibody to prevent $TNF-{\alpha}$ induced intestinal damage in the intact animal.

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Role of p38 MAPK in the Regulation of Apoptosis Signaling Induced by TNF-α in Differentiated PC12 Cells

  • Park, Jung-Gyu;Yuk, Youn-Jung;Rhim, Hye-When;Yi, Seh-Yoon;Yoo, Young-Sook
    • BMB Reports
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    • v.35 no.3
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    • pp.267-272
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    • 2002
  • TNF-$\alpha$ elicits various responses including apoptosis, proliferation, and differentiation according to cell type. In neuronal PC12 cells, TNF-$\alpha$ induces moderate apoptosis while lipopolysarccaharide or trophic factor deprivation can potentiate apoptosis that is induced by TNF-$\alpha$. TNF-$\alpha$ initiates various signal transduction pathways leading to the activation of the caspase family, NF-${\kappa}B$, Jun N-terminal kinase, and p38 MAPK via the death domain that contains the TNF-$\alpha$ receptor. Inhibition of translation using cycloheximide greatly enhanced the apoptotic effect of TNF-$\alpha$. This implies that the induction of anti-apoptotic genes for survival by TNF-$\alpha$ may be able to protect PC12 cells from apoptosis. Accordingly, Bcl-2, an anti-apoptotic genes for survival by TNF-$\alpha$ may be able to protect PC12 cells from apoptosis. Accordingly, Bcl-2, an anti-apoptotic Bcl-2 family member, was highly expressed in response to TNF-$\alpha$. In this study, we examined the anti-apoptotic role of p38 MAPK that is activated by TNF-$\alpha$ in neuronal PC12 cells. The phosphorylation of p38 MAPK in response to TNF-$\alpha$ slowly increased and lasted several hours in the PC12 cell and DRG neuron. This specific inhibitor of p38 MAPK, SB202190, significantly enhanced the apoptosis that was induced by TNF-$\alpha$ in PC12 cells. This indicates that the activation of p38 MAPK could protect PC12 cells from apoptosis since there is no known role of p38 MAPK in resoonse to TNF-$\alpha$ in neuron. This discovery could be evidence for the neuroprotective role of the p38 MAPK.

The Effect of Tumor Necrosis Factor-Alpha on Glomerular Epithelial Cells in Glomerular Permeability ($TNF-{\alpha}$가 토리 상피세포의 투과성에 미치는 영향)

  • Cho Min-Hyun;Lee Ji-Hye;Koo Ja-Hoon;Ko Cheol-Woo
    • Childhood Kidney Diseases
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    • v.8 no.1
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    • pp.1-9
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    • 2004
  • Purpose : Minimal Change Disease (MCD) is the most common primary nephrotic syndrome in children. Some suggested that tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$) are involved in the pathogenesis of MCD. Methods : This study was done to see the changes of plasma and urinary $TNF-{\alpha}$, and its effect on the determination of permeability of the glomerular basement membrane (BM) contributed by heparan sulfate proteoglycan (HSPG). Study patients consisted of 19 biopsy-proven MCD children aged 2-15 years old. Both plasma and urinary $TNF-{\alpha}$ were measured. Employing the Millicell system, $TNF-{\alpha}$ was screened for the permeability factors. We examined whether $TNF-{\alpha}$ regulated BM HSPG gene expression and HS synthesis in the glomerular epithelial cells (GECs). Results : Urinary $TNF-{\alpha}$ during relapse was significantly increased when compared with that of during remission or controls ($364.4{\pm}51.2$ vs $155.3{\pm}20.8,\;36.0{\pm}4.5$ ng/mg cr) (P<0.05). However, negative results were obtained in the permeability assay using the Millicell system. No difference was seen in the BM HSPG gene expression and HS synthesis in the GECs. Conclusion : It seems that $TNF-{\alpha}$ may not play a disease-specific role in the pathogenesis of MCD.

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Differential Effects of TNF-${\alpha}$ on the Survival and Apoptosis of Human Granulocytes and the Human Myeloid Leukemia Cell Line

  • Yang, Eun Ju;Chang, Jeong Hyun
    • Biomedical Science Letters
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    • v.19 no.2
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    • pp.118-123
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    • 2013
  • Tumor necrosis factor-alpha (TNF-${\alpha}$) is a proinflammatory cytokine that mediates the inflammatory response and immune functions, and modulates the proliferation, differentiation and cell death of cancer cells. The differential functions of TNF-${\alpha}$ in various human cells due to the formation of different stimulating pathway upon the binding of TNF-${\alpha}$ to its receptors. In the present study, we examined the different effects of TNF-${\alpha}$ on the survival and apoptosis between normal granulocytes and human myeloid leukemia HL-60 cells. Although TNF-${\alpha}$ did not affect on the constitutive apoptosis of granulocytes, TNF-${\alpha}$ strongly induced the apoptosis of HL-60 cells in a dose- and a time-dependent manner. TNF-${\alpha}$-induced apoptosis was occurred via the activation of caspase 8, caspase 9 and caspase 3/7 and the induction of ROS production in HL-60 cells. Also, BAY-11-7085, a NF-${\kappa}B$ inhibitor, blocked the TNF-${\alpha}$-induced apoptosis in HL-60 cells. NF-${\kappa}B$ may be involved in TNF-${\alpha}$-induced apoptotic signaling pathway in HL-60 cells. These results suggest that TNF-${\alpha}$ activates apoptotic pathways and its process depends on cell type and many cellular factors. A better understanding of the differential effect of TNF-${\alpha}$ on cell apoptosis and survival may provide important information that can be used to elucidate the specific inhibitory effect of TNF-${\alpha}$ on the cancer dis.

Expression of a Functional Human Tumor Necrosis Factor-${\alpha}$ (hTNF-$\alpha$) in Yeast Saccharomyces cerevisiae

  • Park, Seung-Moon;Mo, Ae-Young;Jang, Yong-Suk;Lee, Jae-Hwa;Yang, Moon-Sik;Kim, Dae-Hyuk
    • Biotechnology and Bioprocess Engineering:BBE
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    • v.9 no.4
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    • pp.292-296
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    • 2004
  • The recombinant soluble human tumor necrosis factor-alpha (hTNF-$\alpha$) was expressed in a yeast Saccharomyces cerevisiae and its cytotoxicity was evaluated. A cDNA encoding hTNF-$\alpha$ was placed under the control of two different promoters: a glyceraldehyde-3-phosphate dehydrogenase (GPD) promoter and a yeast hybrid ADH2-GPD promoter, consisting of alcohol dehydrogenase II (ADH2) and the GPD promoter. A Northern blot analysis revealed that, although variation in the expression level of hTNF-$\alpha$ existed among transformants, the higher expression was obtained with the GPD promoter. Expressed hTNF-$\alpha$ protein (rhTNF-$\alpha$) was successfully secreted into the culture medium, producing 2.5 mg per liter of culture filtrate, with no changes in cell growth. The bioassay for observing the cytotoxicity to the murine L929 fibroblast cell line, with serial dilution of rhTNF-$\alpha$, indicated that the secreted rhTNF-$\alpha$ was bioactive and its dose-response was improved eight to ten times over that of the E. coli-derived rhTNF-$\alpha$.

Changes of Plasma and Urinary $TNF-{\alpha}$ in Children with Minimal Change Nephrotic Syndrome and Its Role in Albumin Permeability (미세변화신증후군 환아에서 Tumor Necrosis Factor-${\alpha}$의 혈중 및 요중 변화와 알부민 투과성에 미치는 영향)

  • Cho Min-Hyun;Lee Hwan-Seok;Oh Hyun-Hee;Chung Ki-Young;Koo Ja-Hoon;Ko Cheol-Woo
    • Childhood Kidney Diseases
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    • v.7 no.1
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    • pp.16-22
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    • 2003
  • Purpose : Minimal Change Disease(MCD) is the most common primary nephrotic syndrome in children. Some suggested that tumor necrosis factor-${\alpha}$ ($TNF-{\alpha}$) are involved in the pathogenesis of MCD. This study was done to see the changes of plasma and urinary $TNF-{\alpha}$, and their effects on the permeability of glomerular basement membrane. Methods : Study patients consisted of 19 biopsy-proven MCD children aged 2-15 years old. Both plasma and urinary $TNF-{\alpha}$ were measured. Employing the Millicell system, $TNF-{\alpha}$ were screened for the permeability factors. Results : Urinary $TNF-{\alpha}$ during relapse was significantly increased(P<0.01). No significant change was seen in the plasma $TNF-{\alpha}$ during relapse when compared to those in remission and the healthy controls. Furthermore, in the in vitro Millicell system, $TNF-{\alpha}$ did not produce a significant change in albumin permeability. Conclusion : Therefore, it seems that $TNF-{\alpha}$ may not play a disease-specific role in the pathogenesis of MCD.

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Molecular Mechanisms Involved in Peptidoglycan-induced Expression of Tumor Necrosis Factor-α in Monocytic Cells (펩티도글리칸에 의한 단핵세포의 Tumor necrosis factor-α 발현 기전 연구)

  • Jeong, Ji-Young;Son, Yonghae;Kim, Bo-Young;Kim, Koanhoi
    • Journal of Life Science
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    • v.29 no.11
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    • pp.1251-1257
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    • 2019
  • Peptidoglycan (PG) is found in atheromatous lesions of arteries, where monocytes/macrophages express inflammatory cytokines, including tumor necrosis factor-alpha ($TNF-{\alpha}$). This study investigated the effects of PG on $TNF-{\alpha}$ expression and examined possible cellular factors involved in $TNF-{\alpha}$ upregulation. The overall aim was to identify the molecular mechanisms underlying inflammatory responses to bacterial pathogen-associated molecular patterns in the artery. Exposure of human THP-1 monocytic cells to PG enhanced the secretion of $TNF-{\alpha}$ and induced its gene transcription. Inhibition of TLR-2/4 with OxPAPC significantly inhibited $TNF-{\alpha}$ gene expression, whereas inhibition of LPS by polymyxin B did not. The PG-induced expression of $TNF-{\alpha}$ was also significantly suppressed by pharmacological inhibitors that modulate activities of cellular signaling molecules; for example, U0126 (an ERK inhibitor), SB202190 (a p38 MAPK inhibitor), and SP6001250 (a JNK inhibitor) significantly attenuated PG-induced transcription of $TNF-{\alpha}$ and secretion of its gene product. $TNF-{\alpha}$ expression was also inhibited by rapamycin (an mTOR inhibitor), LY294002 (a PI3K inhibitor), and Akt inhibitor IV (an Akt inhibitor). ROS-regulating compounds, like NAC and DPI, also significantly attenuated $TNF{\alpha}$ expression induced by PG. These results suggest that PG induces $TNF-{\alpha}$ expression in monocytes/macrophages by multiple molecules, including TLR-2, PI3K, Akt, mTOR, MAPKs, and ROS.

Clinical Study of the Correlation of Tumor Necrosis Factor Alpha and the Proteinuria of Henoch-Schönlein Nephritis and Idiopathic Nephrotic Syndrome (Henoch-Schönlein Purpura 신염과 특발성 신증후군에서 Tumor Necrosis Factor Alpha와 단백뇨와의 관련성에 관한 임상적 연구)

  • Jeong, Dong-Ho;Park, Jeong-Hyun;Jeong, Hye-Cheon;Koo, Hyun-Hoe;Lee, Jun-Ho;Ha, Tae-Sun
    • Korean Journal of Pediatrics
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    • v.45 no.2
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    • pp.240-246
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    • 2002
  • Purpose : It is not clear that the development of glomerular injury and aggravation by tumor necrosis factor alpha($TNF-{\alpha}$) is related to intrarenal or serum concentration of $TNF-{\alpha}$. So, we studied the relationship between the concentration of $TNF-{\alpha}$ and aggravation of glomerular damage in the Henoch-$Sch{\ddot{o}}nlein$ nephritis(HSN) and idiopathic nephrotic syndrome(INS). Methods : We collected the sera and urines of 21 patients with Henoch-$Sch{\ddot{o}}nlein$ purpura(HSP) and 22 patients with INS visited Chungbuk National University hospital from March 1998 to March 2001. The concentration of $TNF-{\alpha}$ in the sera and urines were measured by sandwich ELISA. Results : Serum $TNF-{\alpha}$ levels in the HSP patients with renal involvement were significantly higher than those without renal involvement(P=0.009). But urine $TNF-{\alpha}$ levels have no correlation with renal involvement(P=0.088). In the HSN patients, proteinuria have a significant correlation with serum $TNF-{\alpha}$ levels(P=0.004) but less correlation with urine $TNF-{\alpha}$ levels(P=0.053). Otherwise, proteinuria have no correlation with serum $TNF-{\alpha}$ levels(P=0.763) but have a significant correlation with urine $TNF-{\alpha}$ levels(P=0.007) in INS. Conclusion : These result suggest that the serum concentration of $TNF-{\alpha}$ would be important to glomerular involvement in HSP. And, it is interesting that proteinuria shows a significant relation with serum $TNF-{\alpha}$ levels in the HSN, but with urine $TNF-{\alpha}$ levels in the INS. This means the major production of $TNF-{\alpha}$ may be originated by extrarenal inflammation in the HSN and by intrarenal tubulo-interstitial damage due to proteinuria in the INS.