• Journal of Microbiology
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• v.39 no.3
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• pp.181-185
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• 2001

The morphological characteristics of newly isolated Cordyceps hepialidicola were characterized, and the phylogenetic relationships with other Cordyceps species were investigated using a sequence analysis of the internal transcribed spacer (ITS). The PCR product of 592 bp showed a homology of 92 and 91% with C. militaris and C. nutans, respectively, In an in vitro model using mouse peripheral blood mononuclear cells (PBMC), a methanol extract of C. hepialidicola induced multiple cytokines, including IFN-${\gamma}$ IL-4, and IL-18. The extract also enhanced the percentages of the CD4$\^$+/ and CD8$\sub$+/ T cells in the healthy murine PBMCs to 56.1% and 13.0%,respectively. The percentages of CD4$\^$+/ and CD8$\^$+/ in the untreated controls were 28.4 and 7.3%, and concanavalin A-treated positive controls were 62.4 and 18.3%, respectively.

• BMB Reports
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• v.49 no.7
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• pp.357-358
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• 2016

Merlin, encoded by the NF2 gene, is a tumor suppressor that exerts its function via inhibiting mitogenic receptors at the plasma membrane. Although multiple mutations in Merlin have been identified in Neurofibromatosis type II (NF2) disease, its molecular mechanism is not fully understood. Here, we show that Merlin interacts with LRP6 and inhibits LRP6 phosphorylation, a critical step for the initiation of Wnt signaling. We found that treatment of Wnt3a caused phosphorylation of Merlin by PAK1, leading to detachment of Merlin from LRP6 and allowing the initiation of Wnt/β-catenin signaling. A higher level of β-catenin was found in tissues from NF2 patients. Enhanced proliferation and migration caused by knockdown of Merlin in glioblastoma cells were inhibited by suppression of β-catenin. Conclusively, these results suggest that sustained Wnt/β-catenin signaling activity induced by abrogation of Merlin-mediated inhibition of LRP6 phosphorylation might be a cause of NF2 disease.

• Asian-Australasian Journal of Animal Sciences
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• v.21 no.3
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• pp.456-464
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• 2008

Avian and mammalian skeletal muscles exhibit a remarkable ability to adjust to physiological stressors induced by growth, exercise, injury and disease. The process of muscle recovery following injury and myonuclear accretion during growth is attributed to a small population of satellite cells located beneath the basal lamina of the myofiber. Several metabolic factors contribute to the activation of satellite cells in response to stress mediated by illness, injury or aging. This review will describe the regenerative properties of satellite cells, the processes of satellite cell activation and highlight the potential role of satellite cells in skeletal muscle growth, tissue engineering and meat production.

• YAKHAK HOEJI
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• v.38 no.4
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• pp.418-424
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• 1994

Lectin from mistletoe (Viscum coloratum) were obtained by salt fractionation, gel filtration and anion exchange chromatography. A molecular weight of about 60,000D has been determined by SDS-PAGE and two basic subunits which have molecular weights of 33,000D and 28,000D are linked by a disulfide bond. The partially purified mistletoe lectins agglutinated human B erythrocytes. Agglutinating activity was relatively stable at varied pH $(3.77{\sim}8.71)$ and at temperature range of $0{\sim}40^{\circ}C$ and not affected by 9 metal ions. Galactose, lactose and N-acetyl-D- galactosamine inhibited agglutinating activity of lectin. Lectin from mistletoe was more mitogenic to murine lymphocytes than concanavalin A.

• Archives of Pharmacal Research
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• v.15 no.4
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• pp.379-381
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• 1992

Phellinus linteus was examined on its immunostimulating activities using an in vitro imunization and plaque forming cell assay. When lymphocytes were exposed to the extract of Phellinus linteus, the number of antibody forming cell was increased. In in vitro plaque forming cell assay, the immunostimulating effect was about 4.8 and 5.0 times of unimmunized control in polyconal and T-independent antibody response, respectively. Especially, Phellinus linteus significantly increased the antigenicity of TNP-LPS used as T-independent antigen. But Phellinus linteus did now show a mitogenic effect on B-lymphcytes. These results suggest that immunostimulating activity of Phillinus lintues might be associated with a functional stimulation of B-lympohocyte involved in humoral immune response.

• Korean Journal of Veterinary Research
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• v.31 no.4
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• pp.433-440
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• 1991

Guinea pigs were administrated with T-2 toxin at a rate of 1 and 0.6mg/kg body weight per day for 21 days to study the immunological and pathological effects of T-2 toxin in guinea pigs. Blood was collected before T-2 treatment and on days 7, 14 and 21 of the trial for hematological and biological examinations and for the mitogen assay using lymphocytes. Myeloid: erythroid ratios were examined from the fernur bone marrow samples taken a day before T-2 toxin treatment began, on day 12 and at death. Guinea pigs received with 1mg/kg body weight of T-2 toxin daily showed leukopenic, lymphopenic and anemic signs on day 7 and 14. The mitogenic responses to the T-cell mitogen, Concanavalin A and B-cell mitogens, lipopolysaccharide were significantly depressed on day 7. Histologically, marked cellular damages including karyorrhexis and depletion of lymphocytes were observed in the actively dividing cells of the gastrointestinal tract, lymph node, spleen and bone marrow of guinea pigs.

• Journal of Microbiology
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• v.44 no.3
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• pp.320-326
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• 2006

Pasteurella multocida is an important veterinary and opportunistic human pathogen. In particular, strains of P. multocida serogroup D cause progressive atrophic rhinitis, and produce a potent, intracellular, mitogenic toxin known as P. multocida toxin (PMT), which is encoded by the toxA gene. To further investigate the toxigenic and pathogenic effects of PMT, a toxA-deleted mutant was developed by homologous gene recombination. When administrated to mice, the toxigenicity of the toxA mutant P. multocida was drastically reduced, suggesting that the PMT constributes the major part of the toxigenicity of P, multocida. Similar results were obtained in a subsequent experiment, while high mortalities were observed when toxA(+) P. multocida bacterial culture or culture Iysate were administrated. Mice immunized with toxA(-) P. multocida were not protected (none survived) following challenge with toxA(+) P. multocida or bacterial culture Iysate (toxin). These results suggest that the toxigenicity of P. multocida is mainly derived from PMT.

• YAKHAK HOEJI
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• v.31 no.4
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• pp.213-218
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• 1987

Twenty species of higher fungi growing in the wild were collected and studied extensively for their lectin activities by using erythrocytes of human, rabbit and mouse blood. In total, 14 species demonstrated hemagglutination with some kinds of erythrocytes. Of twenty species, eight (Boletus edulis, B. splendidus, Clavaria zollingeri, Lactaritis subzonarius, L. volemus, Russula cutefracta, Pholiota squarrosa, and P. aspera) were shown lymphoagglutination with murine splenic lymphocytes. Protein contents were estimated from the crude lectin fraction. Above mentioned eight species contained relatively high amounts of proteins than other mushrooms. Since these species had coincidently, hiig emagglutinating activity as well, we could define them as lectin-containeing mushrooms. Some species also contained mitogenic lectins toward murine splenic lymphocytes.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.248.1-248.1
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• 2003

Keloids are characterized by abnormal proliferation of fibroblasts and overproduction of collagen. Recently, it is reported that transforming growth factor beta (TGFb) and its signaling molecule, SMAD3 are related to the mitogenic effect of fibroblasts and a stimulatory factor for collagen synthesis. Cationic SLN was developed to improve the complex formation of DNA/SLN and enhance the uptake efficiency to cells. SLN was formulated by DC-Chol, DOPE, trimyristin as a solid core and other surfactant. The physical properties of the SLN and the ATS-SLN complex were characterized. (omitted)

• Proceedings of the Korean Nutrition Society Conference
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• 1995.11b
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• pp.11-34
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• 1995

Growth hormone (GH) plays a key role in regulating postnatal growth and can stimulate growth of animals by acting directly on specific receptors on the plasma membrane of tissues or indirectly through stimulating insulin-like growth factor (IGF)-I synthesis and secretion by the liver and other tissues. IGF-I and IGF-Ⅱ are polypeptides with structural similarity with proinsulin that stimulate cell proliferation by endocrine, paracrine and autocrine mechanisms. The initial event in the metabolic action of IGFs on target cells appears to be their binding to specific receptors on the plasma membrane. Current evidence indicates that the mitogenic actions of both IGFs are mediated primarily by binding to the type I IGF receptors, and that IGF action is also mediated by interactions with IGF-binding proteins (IGFBPs). Six distinct IGFBPs have been identified that are characterized by cell-specific interaction, transcriptional and post-translational regulation by many different effectors, and the ability to either potentiate or inhibit IGF actions. Nutritional deficiencies can have their devastating consequence during growth. Although IGF-I is the major mediator of GH's action on somatic growth, nutritional status of an organism is a critical regulator of IGF-I and IGFBPs. Various nutrient deficiencies result in decreased serum IGF-I levels and altered IGFBP levels, but the blood levels of GH are generally unchanged or elevated in malnutrition. Effects of protein, energy, vitamin C and D, and zinc on serum IGF and IGFBP levels and tissue mRNA levels were reviewed in the text. Multiple factors are involved in the regulation of intestinal epithelial cell growth and differentiation. Among these factors the nutritional status of individuals is the most important. The intestinal epithelium is an important site for mitogenic action of the IGFs in vivo, with exogenous IGF-I stimulating mucosal hyperplasia. Therefore, the IGF system appears to provide and important mechanism linking nutrition and the proliferation of intestinal epithelial cells. In order to study the detailed mechanisms by which intestinal mucosa is regulated, we have utilized IEC-6 cells, an intestinal epithelial cell line and Caco-2 cells, a human colon adenocarcinoma cell line. Like intestinal crypt cells analyzed in vivo or freshly isolated intestinal epithelial cells, IEC-6 cells and Caco-2 cells possess abundant quatities of both type Ⅰ and type Ⅱ IGF receptors. Exogenous IGFs stimulate, whereas addition of IGFBP-2 inhibits IEC-6 cell proliferation. To investigate whether endogenously secreted IGFBP-2 inhibit proliferation, IEC-6 cells were transfected with a full-length rat IGFBP-2 cDNA anti-sense expression construct. IEC-6 cells transfected with anti-sense IGFBP-2 protein in medium. These cells grew at a rate faster than the control cells indicating that endogenous IGFBP-2 inhibits proliferation of IEC-6 cells, probably by sequestering IGFs. IEC-6 cells express many characteristics of enterocyte, but do not undergo differentiation. On the other hand, Caco-2 cells undergo a spontaneous enterocyte differentiation. On the other hand, Caco-2 cells undergo a spontaneous enterocyte differentiation after reaching confluency. We have demonstrated that Caco-2 cells produce IGF-Ⅱ, IGFBP-2, IGFBP-3, and an as yet unidentified 31,000 Mr IGFBP, and that both mRNA and peptide secretion of IGFBP-2 and IGFBP-3 increased, but IGFBP-4 mRNA and protein secretion decreased after the cells reached confluency. These changes occurred in parallel to and were coincident with differentiation of the cells, as measured by expression of sucrase-isomaltase. In addition, Caco-2 cell clones forced to overexpress IGFBP-4 by transfection with a rat IGFBP-4 cDNA construct exhibited a significantly slower growth rate under serum-free conditions and had increased expression of sucrase-isomaltase compared with vector control cells. These results indicate that IGFBP-4 inhibits proliferation and stimulates differentiation of Caco-2 cells, probably by inhibiting the mitogenic actions of IGFs.