• IMMUNE NETWORK
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• 제1권3호
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• pp.260-265
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• 2001

Transforming growth $factor-{\beta}1$ ($TGF-{\beta}1$) is a multipotent growth factor affecting development, homeostasis and tissue repair. Many kinds of malignant tissues were reported to overexpress transforming growth $factor-{\beta}1$ ($TGF-{\beta}1$) gene. However, a little work has been done on the circulating $TGF-{\beta}1$ and the association of $TGF-{\beta}1$ with progression in patients with malignant tumors. In this study, we measured the plasma level of $TGF-{\beta}1$ in gastric cancer and prostate cancer patients and evaluated the utility of plasma $TGF-{\beta}1$ as a possible tumor marker. We used Enzyme-linked immunosorbent assay (ELISA) system in order to measure plasma $TGF-{\beta}1$ level in 134 gastric cancer patients, 50 prostate cancer patients and 290 normal controls. And the tumor marker, carcinoembryonic antigen (CEA), prostate-specific antigen (PSA), was compared with $TGF-{\beta}1$ in the aspects of sensitivity and specificity. The mean plasma $TGF-{\beta}1$ levels were $1.219{\pm}0.834$ (0.272-5.772) ng/mL in normal controls, $5.964{\pm}3.218$ (0.845-18.124) ng/mL in gastric cancer and $4.140{\pm}2.345$ (1.108-13.302) ng/mL in prostate cancer. In gastric cancer patients difference in plasma $TGF-{\beta}1$ level was not detected according to cancer stage. In comparison with other tumor marker (CEA, PSA) $TGF-{\beta}1$ is more potent in sensitivity. These results indicate that the plasma $TGF-{\beta}1$ level can be a potent tumor marker in gastric cancer and prostate cancer.

• Tuberculosis and Respiratory Diseases
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• 제73권2호
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• pp.84-92
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• 2012

Background: Asian dust storms can be transported across eastern Asia. In vitro, Asian dust particle-induced inflammation and enhancement of the allergic reaction have been observed. However, the fibrotic effects of Asian dust particles are not clear. Production of transforming growth factor ${\beta}_1$ (TGF-${\beta}_1$) and fibronectin were investigated in the bronchial epithelial cells after exposure to Asian dust particulate matter (AD-PM10). Methods: During Asian dust storm periods, air samples were collected. The bronchial epithelial cells were exposed to AD-PM10 with and without the antioxidant, N-acetyl-L-cysteine (NAC). Then TGF-${\beta}_1$ and fibronectin were detected by Western blotting. The reactive oxygen species (ROS) was detected by the measurement of dicholorodihydrofluorescin (DCF), using a FACScan, and visualized by a confocal microscopy. Results: The expression of TGF-${\beta}_1$, fibronectin and ROS was high after being exposed to AD-PM10, compared to the control. NAC attenuated both TGF-${\beta}_1$ and fibronectin expression in the AD-PM10-exposed the bronchial epithelial cells. Conclusion: AD-PM10 may have fibrotic potential in the bronchial epithelial cells and the possible mechanism is AD-PM10-induced intracellular ROS.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• 제32권1호
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• pp.8-18
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• 2006

Purpose: The purpose of this study was to verify that the expressions of angiogenin, transforming growth factor-beta(TGF-${\beta}$), vascular endothelial growth factor(VEGF), human apurinic/apyrimidinic endonuclease(APEX) and tumor necrosis factor-alpha(TNF-${\alpha}$) were associated with the tumorigenesis of the oral squamous cell carcinoma(OSCC). Materials and Methods: Fifty-one samples of OSCC and fifteen normal oral mucosae were obtained to analyze the expression levels of above five factors. mRNA expressions were quantified by the quantitative competitive PCR(QC-PCR) method. After 2% agarose gel electrophoresis stained with ethidium bromide, the concentration of mRNA was calculated by a digital image analysis system. The expression levels of angiogenin, TGF-${\beta}$, VEGF, APEX and TNF-${\alpha}$ were compared by unpaired Student's t-tests between cancer and normal tissues. We analyzed statistically to find the cut-off values that would be useful as diagnostic markers, and the linear regression analysis between every two factors of these five factors by SAS system. Results: All of these five factors (angiogenin: P<0.0037, TGF-${\beta}$: P<0.0001, VEGF: P<0.0102, APEX: P<0.0023, TNF-${\alpha}$: P<0.0074) were significantly correlated with OSCC. In the analysis to find the cut-off values for the diagnosis, we could not find any value that had a reasonable sensitivity and specificity. In the linear regression analysis, there were correlations between angiogenin and TNF-${\alpha}$, TGF-${\beta}$ and VEGF, TGF-${\beta}$ and APEX, TGF-${\beta}$ and TNF-${\alpha}$, VEGF and APEX, VEGF and TNF-${\alpha}$, APEX and TNF-${\alpha}$. Conclusion: Our results suggest that not only angiogenin, TGF-${\beta}$, VEGF, APEX and TNF-${\alpha}$ are significantly associated with the tumorigenesis, but also the close relationship between these factors might enhance the tumorigenesis of OSCC. We can not find clinical availability for diagnosis.

• 치위생과학회지
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• 제12권6호
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• pp.689-695
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• 2012

The aim of this study was to elucidate the effects of concentrated growth factors (CGFs) on human gingival fibroblasts in vitro. Blood was collected from three male volunteers (average age 27 years). CGFs were prepared using standard protocols. The CGF exudates were collected at the following culture time points: 1, 7, 14, and 21 days. The levels of platelet-derived growth factor BB (PDGF-BB) and transforming growth factor ${\beta}1$ (TGF-${\beta}1$) in CGFs were quantified. The CGF exudates were then used to culture human gingival fibroblasts. The biologic characteristics of these fibroblasts were analyzed in vitro for 21 days. Platelet-rich plasma released the highest amounts of TGF-${\beta}1$ and PDGF-BB on the first day. The level of TGF-${\beta}1$ had decreased slightly by day 7, although the difference compared to levels at day 1 was not statistically significant. However, by days 14 and 21, levels of TGF-${\beta}1$ had dropped significantly compared to day 1 levels. The levels of PDGF-BB at days 7, 14, and 21 did not differ significantly from that measured on day 1. CGFs maintained the release of autologous growth factors for a reasonable period of time (7 days for TGF-${\beta}1$ and 21 days for PDGF-BB). Gingival fibroblasts treated with CGF exudates collected at day 14 reached peak viability and synthesized type I collagen. Furthermore, the CGF exudates exerted positive effects on the proliferation and differentiation of these cells at days 1, 7, 14, and 21. The findings of this study suggest that treatment with CGFs represents a promising method of enhancing mucosal healing following surgical procedures.

• Journal of Ginseng Research
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• 제43권1호
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• pp.68-76
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• 2019

Background: In colorectal cancer (CRC), 40-60% of patients develop metastasis. The epithelial-mesenchymal transition (EMT) is a pivotal and intricate process that increases the metastatic potential of CRC. The aim of this study was to investigate the effect of Korean Red Ginseng extract (RGE) on colorectal metastasis through inhibition of EMT and the metastatic abilities of CRC cells. Methods: To investigate the effect of RGE on the metastatic phenotypes of CRC cells, CT26 and HT29 cells were evaluated by using an adhesion assay, a wound-healing assay, an invasion assay, zymography, and real-time reverse transcription-polymerase chain reaction. Western-blot analysis was conducted to elucidate the molecular mechanisms of RGE, which showed an inhibitory effect on the transforming growth factor-${\beta}1$ ($TGF-{\beta}1$)-induced EMT in HT29 cells. Additionally, the antimetastatic effect of RGE was evaluated in a mouse model of lung metastasis injected with CT26 cells. Results: RGE decreased the adhesion and migration ability of the CT26 cells and TGF-${\beta}1$-treated HT29 cells. The invasion ability was also reduced by RGE treatment through the inhibition of matrix metalloproteinase-9 expression and activity. Moreover, RGE suppressed the TGF-${\beta}1$-induced EMT via TGF-${\beta}1$/Smad-signaling-mediated Snail/E-cadherin expression in HT29 cells and lung tissue in CT26 tumor-bearing mice. Conclusion: Our results demonstrated that RGE inhibited colorectal lung metastasis through a reduction in metastatic phenotypes, such as migration, invasion, and the EMT of CRC cells.

• Tuberculosis and Respiratory Diseases
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• 제43권2호
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• pp.164-172
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• 1996

연구배경 : TGF-$\beta$는 25kD의 단백으로써, 폐섬유증의 병인에 있어 TGF-$\beta$의 발현과 밀접한 관계가 있다고 보고되고 있다. TGF-$\beta$는 세포외 분자들의 합성 및 생산을 촉진할 뿐만아니라 세포간질의 붕괴를 감소시킨다. 특발성 폐섬유증을 포함한 다른원인에 의한 간질성 폐질환의 폐섬유증에 있어 TGF-$\beta$의 발현양상은 상향조절된다고 알려져 있다. 연구방법 : 본연구는 특발성 폐섬유증과, bleomycin, 유육종증, 및 폐의 호산구성 육아종에 의한 간질성 폐질환에 있어서 TGF-$\beta$의 발현 양상를 연구하고자 개흉 폐생검으로 채취된 특발성 간질성 폐섬유증 3예의 6절편과 폐절제시 채취한 5예의 정상조직을 연구재료로 하였고 bleomycin, 유육종증 및 폐의 호산구성 육아종에 의한 간질성 폐질환환자 각각 3예로부터 얻은 6절편에서 TGF-$\beta$의 단세포군항체를 이용하여 면역조직화학적 검색을 실시하였다 결과 : TGF-$\beta$은 5예의 정상조직의 기관지 상피세포나 폐포세포에서는 약하거나 중등도로 발현되었다. 3예의 특발성 폐섬유증 6절편 중 5절편에서 폐포벽의 간질성 섬유모세포들에서 발현되었고, 1절편에서는 증식된 폐포내 폐포세포에서 발현되었으며 그 정도는 비균질적인 양상을 보였다. 3예의 6절편 중 5절편에서 강한발현을 1절편에서는 중등도의 발현을 나타냈으며 bleomycin이 원인이 되는 간질성 폐질환 6절편중 2절편에서는 중등도의 발현을 4절편에서는 강한발현을 보였고, 유육종증이 원인이 되는 간질성 폐질환 6절편 중 3절편에서 중등도의 발현을, 3절편에서 강한 발현을 보였다. 폐의 호산구성 육이종이 원인이 되는 간질성 폐질환 6절편중 2절편에서 중등도의 발현을, 4절편에서 강한 발현을 보였다. 결론 : TGF-$\beta$의 발현 증가는 특발성 폐섬유증, bleomycin, 유육종증 및 폐의 호산구성 육아종에 의한 간질성 폐질환에 있어서 폐섬유증의 병인과 상당한 관련이 있음을 암시해 주는 것으로 생각된다.

• Journal of Genetic Medicine
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• 제10권1호
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• pp.47-51
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• 2013

Loeys-Dietz syndrome (LDS) is an autosomal dominant disorder caused by heterozygous mutations in the genes encoding transforming growth factor-${\beta}$ receptor type 1 or 2. It is typically characterized by a triad of hypertelorism, cleft palate or bifid uvula, and arterial tortuosity with aneurysm or dissection. Characteristic vascular abnormalities such as tortuosity, aneurysms, dissections, and stenosis are the most severe complications of LDS and can occur in the neurovascular system. We report a 5-year-old boy who presented with headaches and neurovascular abnormalities and was diagnosed with LDS with a novel mutation of the TGFBR1 gene. It is the first Korean report of neurovascular abnormalities in LDS.

• 한국수산과학회지
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• 제49권6호
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• pp.807-814
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• 2016

Fucoidan, one of the dominant sulfated polysaccharides extracted from brown seaweed, possesses a wide range of biological activities. Transforming growth $factor-{\beta}$ ($TGF-{\beta}$) plays a pivotal role in the pathogenesis of pulmonary fibrosis, by stimulating the synthesis of profibrotic factors. In this study, we investigated the in vitro effects of fucoidan on collagen synthesis, ${\alpha}-smooth$ muscle actin (${\alpha}-SMA$) expression, and interleukin (IL)-6 production in $TGF-{\beta}$-stimulated human pulmonary fibroblasts. The expression of type I collagen and ${\alpha}-SMA$ was detected by Western blot, and the production of IL-6 by enzyme-linked immunosorbent assay. $TGF-{\beta}1$ treatment of pulmonary fibroblasts enhanced the expression of ${\alpha}-SMA$, type I collagen, and IL-6 whereas these effects were inhibited in cells pretreated with fucoidan. The activation of Smad2/3, p38 mitogen-activated protein kinases (MAPKs), and Akt was also inhibited in fucoidan-pretreated, $TGF-{\beta}1-stimulated$ human pulmonary fibroblasts. These data demonstrate the anti-fibrotic potential of fucoidan in $TGF-{\beta}-induced$ human pulmonary fibroblasts, via the inhibition of Smad2/3, p38 MAPKs, and Akt phosphorylation. Our results suggest the therapeutic potential of fucoidan in the prevention or treatment of pulmonary fibrosis.

• 대한미생물학회지
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• 제35권5_6호
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• pp.362-362
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• 2000

• The Korean Journal of Physiology and Pharmacology
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• 제12권1호
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• pp.1-6
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• 2008

Ribbon-type antisense oligonucleotide to TGF-${\beta}1$ (TGF-${\beta}1$ RiAS) was designed and tested to prevent or resolve the fibrotic changes induced by $CCl_4$ injection. When Hepa1c1c7 cells were transfected with TGF-${\beta}1$ RiAS, the level of TGF-${\beta}1$ mRNA was effectively reduced. TGF-${\beta}1$ RiAS, mismatched RiAS, and normal saline were each injected to mice via tail veins. When examined for the biochemical effects on the liver, TGF-${\beta}1$ mRNA levels were significantly reduced only in the TGF-${\beta}1$ RiAS-treated group. The results of immunohistochemical studies showed that TGF-${\beta}1$ RiAS prevented the accumulation of collagen and ${\alpha}$-smooth muscle actin, but could not resolve established fibrosis. These results indicate that ribbon antisense to TGF-${\beta}1$ with efficient uptake can effectively prevent fibrosis of the liver.