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- 주제어 : Hepatocyte growth factor (검색결과 75 건)
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Satyakumar Vidyashankar,Sandeep R. Varma,Mohammed Azeemudin,Ashok Godavarthi,Nandakumar S. Krishna,Pralhad Sadashiv Patki 한국식품영양과학회 2011 Journal of medicinal food Vol.14 No.9
Hepatocyte growth factor (HGF) plays an important role in hepatocyte proliferation. HGF expression is regulated by various signaling molecules and nuclear receptors. In the present study, LiverCare^ⓡ (LC), a novel polyherbal formulation (The Himalaya Drug Company, Bangalore, India), was evaluated for its efficacy, using co-cultures of primary rat hepatocytes–non-parenchymal cells (NPCs) and human hepatocellular carcinoma cells (HepG2). The rate of primary hepatocyte co-culture proliferation was significantly and dose-dependently increased by LC as determined by [3H]thymidine incorporation into newly synthesized DNA and cell proliferation assay. LC also increased HGF expression in primary hepatocyte co-culture. Albumin and urea content remained constant during proliferation of hepatocyte co-cultures in the presence of LC with decreased activity of alanine aminotransferase. It is interesting that LC inhibited incorporation of [3H]thymidine into DNA in HepG2 cells. LC enhanced peroxisome proliferator-activated receptor-α expression during hepatocyte proliferation, whereas tumor necrosis factor-α expression remained unaffected. In conclusion, our study clearly showed that LC differentially regulates primary rat hepatocytes and human hepatocarcinoma cell proliferation. LC may be a promising candidate for treating degenerative liver diseases by enhancing liver regeneration.
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Bae, Sung Hae,Ryu, Hoon,Rhee, Ki-Jong,Oh, Ji-Eun,Baik, Soon Koo,Shim, Kwang Yong,Kong, Jee Hyun,Hyun, Shin Young,Pack, Hyun Sung,Im, Changjo,Shin, Ha Cheol,Kim, Yong Man,Kim, Hyun Soo,Eom, Young Woo,L Informa UK Ltd. 2015 Growth factors Vol.33 No.2
<P>L-ascorbic acid 2-phosphate (Asc-2P) acts as an antioxidant and a stimulator of hepatocyte growth factor (HGF) production. Previously, we reported that depletion of growth factors such as fibroblast growth factor (FGF)-2, epidermal growth factor (EGF), FGF-4 and HGF during serial passage could induce autophagy, senescence and down-regulation of stemness (proliferation via FGF-2/-4 and differentiation via HGF). In this study, we investigated the proliferation and differentiation potential of BMSCs by FGF-2 and Asc-2P. Co-treatment with FGF-2 and Asc-2P induced optimal proliferation of BMSCs and increased the accumulation rate of BMSC numbers during a 2-month culture period. Moreover, differentiation potential was maintained by co-treatment with FGF-2 and Asc-2P via HGF expression. Adipogenic differentiation potential by FGF-2 and Asc-2P was dramatically suppressed by c-Met inhibitors (SU11274). These data suggest that co-treatment with FGF-2 and Asc-2P would be beneficial in obtaining BMSCs that possess 'stemness'' during long-term culture.</P>
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Culture with Growth Factor Supplements Improves the Viability and Function of Rat Hepatocytes
나건형,정은선,김동구 대한이식학회 2015 Korean Journal of Transplantation Vol.29 No.3
Background: To identify the optimum culture conditions by investigating isolated rat hepatocytes cultured in medium containing different growth factors. Methods: Hepatocytes were isolated from rats using a two-step perfusion technique and divided into the following four groups cultured in medium containing different growth factors: control, epidermal growth factor (EGF), insulin, and EGF+insulin. The viability of the cultured rat hepatocytes and liver function parameters, including albumin, ammonia, and urea in the culture medium, were measured. Hepatocyte morphology was examined by staining with hematoxylin and eosin, and albumin receptor expression was confirmed by immunofluorescence. Results: Slightly higher viability was observed in the growth factor groups than in the control group, although without significance (P=0.073). The levels of albumin (P=0.001), ammonia (P<0.001), and urea (P=0.041) differed significantly among the four groups. The functional parameters in the growth factor groups, particularly the EGF+insulin group, were significantly superior to those in the control group. The morphology of the hepatocytes in all growth factor groups was well maintained at 10 days. However, the control group showed deterioration in cell morphology by day 7. Conclusions: Morphological and functional assessment indicated that the presence of growth factors, particularly EGF+insulin, provided culture conditions superior to those of non-supplemented medium.
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Expression of Hepatocyte Growth Factor/c-met by RT-PCR in Meningiomas
김나래,채양석,임원정,조성진 대한병리학회 2011 Journal of Pathology and Translational Medicine Vol.45 No.5
Background: Hepatocyte growth factor (HGF) is a potent mitogenic cytokine. C-met protein, which is known to be the HGF receptor has transmembrane tyrosine kinase activity and is encoded by the c-met oncogene. The HGF/c-met signaling pathway may play various roles in the carcinogenesis of various organs. Methods: We examined HGF and c-met mRNA expression by utilizing reverse transcription polymerase chain reaction on 40 surgically resected intracranial meningiomas (25 benign, 10 atypical, and 5 anaplastic cases). Results: An HGF overexpression was detected in 28%, 50%, and 80% of the benign, atypical and anaplastic meningiomas, respectively; a high expression of HGF or the coexpression of HGF/c-met was detected in the high grade meningiomas (the atypical and anaplastic cases, p=0.046, p=0.014). An HGF expression was statistically significant in the recurrent meningiomas (p=0.003), and HGF expression was significantly lower than c-met mRNA expression in benign meningiomas (p=0.034). Conclusions: There was no correlation between histologic subtypes and HGF/c-met expression. Determination of HGF expression can be used as a molecular predictor for recurrence of meningioimas. These results suggest that HGF and c-met expression in meningiomas may be associated with anaplastic progression.
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Prohibitin 1 Regulates the H19-Igf2 Axis and Proliferation in Hepatocytes
Ramani, Komal,Mavila, Nirmala,Ko, Kwang Suk,Mato, José,M.,Lu, Shelly C. American Society for Biochemistry and Molecular Bi 2016 The Journal of biological chemistry Vol.291 No.46
<P>Prohibitin 1 (PHB1) is a mitochondrial chaperone that regulates cell growth. Phb1 knock-out mice exhibit liver injury and hepatocellular carcinoma (HCC). Phb1 knock-out livers show induction of tumor growth-associated genes, H19 and insulin-like growth factor 2 (Igf2). These genes are controlled by the imprinting control region (ICR) containing CCCTC-binding transcription factor (CTCF)-binding sites. Because Phb1 knock-out mice exhibited induction of H19 and Igf2, we hypothesized that PHB1-mediated regulation of the H19-Igf2 axis might control cell proliferation in normal hepatocytes. H19 and Igf2 were induced (8-20-fold) in 3-week-old Phb1 knock-out livers, in Phb1 siRNA-treated AML12 hepatocytes (2-fold), and HCC cell lines when compared with control. Phb1 knockdown lowered CTCF protein in AML12 by approximate to 30% when compared with control. CTCF overexpression lowered basal H19 and Igf2 expression by 30% and suppressed Phb1 knockdown-mediated induction of these genes. CTCF and PHB1 co-immunoprecipitated and co-localized on the ICR element, and Phb1 knockdown lowered CTCF ICR binding activity. The results suggest that PHB1 and CTCF cooperation may control the H19-Igf2 axis. Human HCC tissues with high levels of H19 and IGF2 exhibited a 40-50% reduction in PHB1 and CTCF expression and their ICR binding activity. Silencing Phb1 or overexpressing H19 in the mouse HCC cell line, SAMe-D, induced cell growth. Blocking H19 induction prevented Phb1 knockdown-mediated growth, whereas H19 overexpression had the reverse effect. Interestingly H19 silencing induced PHB1 expression. Taken together, our results demonstrate that the H19-Igf2 axis is negatively regulated by CTCF-PHB1 cooperation and that H19 is involved in modulating the growth-suppressive effect of PHB1 in the liver.</P>
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구강 및 구인두 편평세포암종에서 Hepatocyte Growth Factor와c-met 유전자 발현의 의의
김진환,오소정,노영수,안회영,신형식,조성진 대한이비인후과학회 2007 대한이비인후과학회지 두경부외과학 Vol.50 No.8
Background and Objectives:The hepatocyte growth factor (HGF)/c-Met signal pathway may play various roles in carcino-genesis of several organs. However, studies about this pathway in head and neck cancers, especially oral cavity and oropharyn-geal squamous cel carcinoma (SCC), are very rare. Our objectives are to evaluate the relationship between the mRNA and protein expression of HGF and c-met genes in oral cavity and oropharyngeal carcinomas. Subjects and Method:examined the mRNA expresion of HGF and c-Met by means of the immunohistochemistry (IHC) method and reverse tran-scription polymerase chain reaction (RT-PCR) in 40 cases of surgically resected oral cavity and oropharyngeal SCC and 10 cases of low grade dysplasia. Results:Using RT-PCR , HGF mRNA amplification was detected in 67.5% and 10% of carcinoma and dysplasia. c-Met mRNA over-expresion was detected in 57.5% and 20% of carcinoma and dysplasia. Using IHC, HGF and Conclusion:These results suggest that HGF/c-Met signal pathway may be associated with the development of oral cavity and oropharyngeal SCC. (Korean J Otorhinolaryngol-Head Neck Surg 2007 ;50 :684-9)
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Kwak, In-Hae,Shin, Yun-Hye,Kim, Myeong-Deok,Cha, Hyun-Young,Nam, Hyun-Ja,Lee, Bok-Soon,Chaudhary, S.C.,Pai, Ki-Soo,Lee, Jae-Ho Korean Society for Biochemistry and Molecular Bion 2011 Experimental and molecular medicine Vol.43 No.2
Aberrant activation of hepatocyte growth factor/scatter factor (HGF/SF) and its receptor, Met, is involved in the development and progression of many human cancers. In the cell-based screening assay, (-)epigallocatechin-3-gallate (EGCG) inhibited HGF/SF-Met signaling as indicated by its inhibitory activity on HGF/SF-induced cell scattering and uPA activation (IC50 = $15.8{\mu}g/ml$). Further analysis revealed that EGCG at low doses specifically inhibited HGF/SF-induced tyrosine phosphorylation of Met but not epidermal growth factor (EGF)-induced phosphorylation of EGF receptor (EGFR). On the other hand, high-dose EGCG decreased both Met and EGFR proteins. We also found that EGCG did not act on the intracellular portion of Met receptor tyrosine kinase, i.e., it inhibited InlB-dependent activation of Met but not NGF-induced activation of Trk-Met hybrid receptor. This inhibition decreased HGF-induced migration and invasion by parental or HGF/SF-transfected B16F10 melanoma cells in vitro in either a paracrine or autocrine manner. Furthermore, EGCG inhibited the invasion/metastasis of HGF/SF-transfected B16F10 melanoma cells in mice. Our data suggest the possible use of EGCG in human cancers associated with dysregulated paracrine or autocrine HGF/SF-Met signaling.
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Ji-Eun Oh,Young Woo Eom 대한의생명과학회 2016 Biomedical Science Letters Vol.22 No.1
Several studies have investigated the various effects of dexamethasone (Dex) on the proliferation and differentiation of mesenchymal stem cells (MSCs). Previously, we reported that co-treatment with L-ascorbic acid 2-phosphate and fibroblast growth factor (FGF)-2 maintained differentiation potential in MSCs through expression of hepatocyte growth factor (HGF). In this study, we investigated the effects of co-treatment with FGF-2 and Dex on the proliferation and differentiation potential of MSCs during a 2-month culture period. Co-treatment with FGF-2 and Dex increased approximately a 4.7-fold higher accumulation rate of MSC numbers than that by FGF-2 single treatment during a 2-month culture period. Interestingly, co-treatment with FGF-2 and Dex increased expression of HGF and maintained adipogenic differentiation potential during this culture period. These results suggest that co-treatment with FGF-2 and Dex preserves the proliferation and differentiation potential during long-term culture.
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In-hae Kwak,이재호,Yun-Hye Shin,Myeongdeok Kim,Hyun-Young Cha,남현자,이복순,CHAUDHARYSHUBHASHCHANDRA,Ki-Soo Pai 생화학분자생물학회 2011 Experimental and molecular medicine Vol.43 No.2
Aberrant activation of hepatocyte growth factor/scatter factor (HGF/SF) and its receptor, Met, is involved in the development and progression of many human cancers. In the cell-based screening assay, (-)epigallocatechin-3-gallate (EGCG) inhibited HGF/SF-Met signaling as indicated by its inhibitory activity on HGF/SF-induced cell scattering and uPA activation (IC50 = 15.8 μg/ml). Further analysis revealed that EGCG at low doses specifically inhibited HGF/SF-induced tyrosine phosphorylation of Met but not epidermal growth factor (EGF)-induced phosphorylation of EGF receptor (EGFR). On the other hand, high-dose EGCG decreased both Met and EGFR proteins. We also found that EGCG did not act on the intracellular portion of Met receptor tyrosine kinase, i.e., it inhibited InlB-dependent activation of Met but not NGF-induced activation of Trk-Met hybrid receptor. This inhibition decreased HGF-induced migration and invasion by parental or HGF/SF-transfected B16F10 melanoma cells in vitro in either a paracrine or autocrine manner. Furthermore, EGCG inhibited the invasion/metastasis of HGF/SF-transfected B16F10 melanoma cells in mice. Our data suggest the possible use of EGCG in human cancers associated with dysregulated paracrine or autocrine HGF/SF-Met signaling.
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