• Development and Reproduction
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• v.23 no.4
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• pp.305-311
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• 2019

Small intestine has a structure called villi that increases the mucosal surface area for nutrient absorption. Intricate and tight epithelial-mesenchymal interactions are required for villi development. These interactions are regulated by signaling molecules, physical forces, and epithelial deformation. Signaling molecules include hedgehog (Hh), bone morphogenetic protein (BMP) and Wnt ligands. The Hh ligand is expressed from the epithelium and binds to the underlying mesenchymal cells, resulting in aggregation into mesenchymal clusters. The clusters express BMP and Wnt ligands to control its size and spacing between clusters. The clusters then form villi. Despite the fact that the villi formation is studied extensively, we do not have a complete understanding. In addition, the recent study shows there is a great relationship between the overexpression of the Hh signal and development of cancer in the gastrointestinal tract. Therefore, signaling between epithelial and mesenchymal cells and their physical interactions will be discussed on this review.

• Molecules and Cells
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• v.27 no.2
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• pp.129-134
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• 2009

Legume plants develop root nodules to recruit nitrogen-fixing bacteria called rhizobia. This symbiotic relationship allows the host plants to grow even under nitrogen limiting environment. Since nodule development is an energetically expensive process, the number of nodules should be tightly controlled by the host plants. For this purpose, legume plants utilize a long-distance signaling known as autoregulation of nodulation (AON). AON signaling in legumes has been extensively studied over decades but the underlying molecular mechanism had been largely unclear until recently. With the advent of the model legumes, L. japonicus and M. truncatula, we have been seeing a great progress including isolation of the AON-associated receptor kinase. Here, we summarize recent studies on AON and discuss an updated view of the long-distance control of nodulation.

• BMB Reports
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• v.41 no.7
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• pp.485-494
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• 2008

The Wnt signaling network, which is composed of Wnt ligands, receptors, antagonists, and intracellular signaling molecules, has emerged as a powerful regulator of cell fate, proliferation, and function in multicellular organisms. Over the past two decades, the critical role of Wnt signaling in embryonic cartilage and bone development has been well established, and much has been learnt regarding the role of Wnt signaling in chondrogenesis and cartilage development. However, relatively little is known about the role of Wnt signaling in adult articular cartilage and degenerative cartilage tissue. This review will briefly summarize recent advances in Wnt regulation of chondrogenesis and hypertrophic maturation of chondrocytes, and review data concerning the role of Wnt signaling in the maintenance and degeneration of articular chondrocytes and cartilage.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.92-93
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• 2003

Chemoprevention refers to the use of agents to inhibit, reverse, or retard tumorigenesis. Numerous phytochemicals present in edible plants have been reported to interfere with a specific stage of the carcinogenic process. Some antioxidative and anti-inflammatory substances derived from dietary or medicinal plants exert chemopreventive properties by targeting intracellular signaling molecules or events.(omitted)

• Journal of Ginseng Research
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• v.44 no.5
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• pp.704-716
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• 2020

Background: Ginsenoside Rh2 (GRh2) is a characterized component in red ginseng widely used in Korea and China. GRh2 exhibits a wide range of pharmacological activities, such as anti-inflammatory, antioxidant, and anticancer properties. However, its effects on Toxoplasma gondii (T. gondii) infection have not been clarified yet. Methods: The effect of GRh2 against T. gondii was assessed under in vitro and in vivo experiments. The BV2 cells were infected with tachyzoites of T. gondii RH strain, and the effects of GRh2 were evaluated by MTT assay, morphological observations, immunofluorescence staining, a trypan blue exclusion assay, reverse transcription PCR, and Western blot analyses. The in vivo experiment was conducted with BALB/c mice inoculated with lethal amounts of tachyzoites with or without GRh2 treatment. Results and conclusion: The GRh2 treatment significantly inhibited the proliferation of T. gondii under in vitro and in vivo studies. Furthermore, GRh2 blocked the activation of microglia and specifically decreased the release of inflammatory mediators in response to T. gondii infection through TLR4/NF-κB signaling pathway. In mice, GRh2 conferred modest protection from a lethal dose of T. gondii. After the treatment, the proliferation of tachyzoites in the peritoneal cavity of infected mice markedly decreased. Moreover, GRh2 also significantly decreased the T. gondii burden in mouse brain tissues. These findings indicate that GRh2 exhibits an antieT. gondii effect and inhibits the microglial activation through TLR4/NF-κB signaling pathway, providing the basic pharmacological basis for the development of new drugs to treat toxoplasmic encephalitis.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2008.04a
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• pp.103-115
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• 2008

Hemodynamic shear stress, the dragging force generated by blood flow, is known as an anti-atherogenic factor. We tested whether lysyl-tRNA synthetase (KRS) will be utilized as an agent controlling shear-sensing systems. KRS was previously known to be secreted as a pro-inflammatory agent. Here we found that KRS inhibited various shear-stimulated signaling pathways. We further found that KRS binds to detergent-resistant membrane (DRM), indicating that KRS binding molecules exist in DRM, specialized regions of the plasma membrane. DRM plays important roles in a variety of cellular processes and consists of gangliosides, signaling molecules and cytoskeletons. We then determined that KRS was colocalized with integrins ${\alpha}4$, ${\alpha}5$ and $av{\beta}3$. In addition, KRS was shown to be associated with sialic acid, existing at the end of gangliosides. Interestingly, the adherent effect of KRS was inhibited by pretreatment with sialic acid. Moreover, treatment of endothelial cells with neuraminidase appeared to inhibit both the KRS adhesion to endothelial cells and shear-stimulated signaling. In conclusion, KRS is likely to be utilized as a vascular regulator.

• Journal of Ginseng Research
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• v.46 no.3
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• pp.489-495
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• 2022

Background: Although ginsenosides and saponins in Korea red ginseng (KRG) shows various pharmacological roles, their roles in the inflammatory response are little known. This study investigated the anti-inflammatory role of ginsenosides identified from KRG saponin fraction (RGSF) and the potential mechanism in macrophages. Methods: The ginsenoside composition of RGSF was identified by high-performance liquid chromatography (HPLC) analysis. An anti-inflammatory effect of RGSF and its mechanisms were studied using nitric oxide (NO) and prostaglandin E₂ (PGE₂) production assays, mRNA expression analyses of inflammatory genes and cytokines, luciferase reporter gene assays of transcription factors, and Western blot analyses of inflammatory signaling pathways using the lipopolysaccharide (LPS)-treated RAW264.7 cells. Results: HPLC analysis identified the types and amounts of various panaxadiol ginsenosides in RGSF. RGSF reduced the generation of inflammatory molecules and mRNA levels of inflammatory enzymes and cytokines in LPS-treated RAW264.7 cells. Additionally, RGSF inhibited the signaling pathways of NF-κB and AP-1 by suppressing both transcriptional factors and signaling molecules in LPS-treated RAW264.7 cells. Conclusion: RGSF contains ginsenosides that have anti-inflammatory action via restraining the NF-κB and AP-1 signaling pathways in macrophages during inflammatory responses.

• Parasites, Hosts and Diseases
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• v.60 no.3
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• pp.155-161
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• 2022

All living organisms are destined to die. Cells, the core of those living creatures, move toward the irresistible direction of death. The question of how to die is critical and is very interesting. There are various types of death in life, including natural death, accidental death, questionable death, suicide, and homicide. The mechanisms and molecules involved in cell death also differ depending on the type of death. The dysenteric amoeba, E. histolytica, designated by the German zoologist Fritz Schaudinn in 1903, has the meaning of tissue lysis; i.e., tissue destroying, in its name. It was initially thought that the amoebae lyse tissue very quickly leading to cell death called necrosis. However, advances in measuring cell death have allowed us to more clearly investigate the various forms of cell death induced by amoeba. Increasing evidence has shown that E. histolytica can cause host cell death through induction of various intracellular signaling pathways. Understanding of the mechanisms and signaling molecules involved in host cell death induced by amoeba can provide new insights on the tissue pathology and parasitism in human amoebiasis. In this review, we emphasized on the signaling role of NADPH oxidases in reactive oxygen species (ROS)-dependent cell death by pathogenic E. histolytica.

• Biomolecules & Therapeutics
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• v.32 no.2
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• pp.192-204
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• 2024

Generally, odorant molecules are detected by olfactory receptors, which are specialized chemoreceptors expressed in olfactory neurons. Besides odorant molecules, certain volatile molecules can be inhaled through the respiratory tract, often leading to pathophysiological changes in the body. These inhaled molecules mediate cellular signaling through the activation of the Ca²⁺-permeable transient receptor potential (TRP) channels in peripheral tissues. This review provides a comprehensive overview of TRP channels that are involved in the detection and response to volatile molecules, including hazardous substances, anesthetics, plant-derived compounds, and pheromones. The review aims to shed light on the biological mechanisms underlying the sensing of inhaled volatile molecules. Therefore, this review will contribute to a better understanding of the roles of TRP channels in the response to inhaled molecules, providing insights into their implications for human health and disease.

• Biomolecules & Therapeutics
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• v.18 no.4
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• pp.363-374
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• 2010

Growing evidence suggests a prominent role for leptin in human cancer progression. The intricate pattern of leptin cross-talk with other associated signaling pathways is a critical area of research that will ultimately contribute to comprehending the role of leptin in cancer progression. This review summarizes a portion of the current understanding of leptin signaling, with a critical focus on its contribution to tumor cell invasion and metastasis. Five topics are addressed in this review: (1) Leptin receptor, (2) Leptin signaling, (3) Leptin and cancer, and (4) Leptin and tumor invasion. Due to the complex cellular effects of leptin, a more precise understanding of leptin signaling pathways must still be elucidated. Leptin is clearly a major factor for stimulating tumor progression through a complex spectrum of interplay and cross-talk among various signaling molecules. An understanding of the role of leptin in invasion and metastasis will provide valuable information for establishing strategies to modulate leptin signaling, which should be a high priority for the development of anti-cancer therapeutics.