• 제목/요약/키워드: Galectin 1

검색결과 41건 처리시간 0.025초

Immunohistochemical localization of galectin-3 in the brain with Theiler's murine encephalomyelitis virus (DA strain) infection

  • Shin, Taekyun;Carrillo-Salinas, Francisco J.;Martinez, Ana Feliu;Mecha, Miriam;Guaza, Carmen
    • 대한수의학회지
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    • 제53권3호
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    • pp.159-162
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    • 2013
  • Galectin-3 is a ${\beta}$-galactoside-binding lectin that plays a role in neuroinflammation through cell migration, proliferation, and apoptosis. In the present study, regulation of galectin-3 was examined in the brain of mice infected with the Daniel strain of Theiler's murine encephalomyelitis virus (TMEV) at days 7 and 81 post-infection by immunohistochemistry. Immunohistochemistry revealed that galectin-3 was mainly localized in ionized calcium-binding adapter 1-positive macrophages/activated microglia, but not in Iba-1-positive ramified microglia. Galectin-3 was also weakly detected in some astrocytes in the same encephalitic lesions, but not in neurons and oligodendrocytes. Collectively, the present findings suggest that galectin-3, mainly produced by activated microglia/macrophages, may be involved in the pathogenesis of virus induced acute inflammation in the early stage as well as the chronic demyelinating lesions in Daniel strain of TMEV induced demyelination model.

Binding Affinities of Carbohydrate-Conjugated Chlorins for Galectin-3

  • Park, Young K.;Bold, Bayarmaa;Cui, Bing Cun;Bai, Jin Quan;Lee, Woo-Kyoung;Shim, Young-Key
    • Bulletin of the Korean Chemical Society
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    • 제29권1호
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    • pp.130-134
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    • 2008
  • Carbohydrate-conjugated chlorins were synthesized for use as biosensors for the detection of the galectin-3 cancer marker. We used ELISA, SDS-gel electrophoresis, and Bradford assays to examine the binding of galectins to d-(+)-galactose- and b-lactose-conjugated chlorins. The binding affinities of these conjugated chlorins for galectin-3 were quantified using fluorescence spectroscopy. The fluorescence emission of the carbohydrate-conjugated chlorins decreased as the amount of galectin-3 in the binding reaction increased over a limited concentration range, indicating that carbohydrate-conjugated chlorins are potentially useful fluorescence biosensors for the galectin-3 cancer marker.

Twist2 Regulates CD7 Expression and Galectin-1-Induced Apoptosis in Mature T-Cells

  • Koh, Han Seok;Lee, Changjin;Lee, Kwang Soo;Park, Eun Jung;Seong, Rho H.;Hong, Seokmann;Jeon, Sung Ho
    • Molecules and Cells
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    • 제28권6호
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    • pp.553-558
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    • 2009
  • In the periphery, a galectin-1 receptor, CD7, plays crucial roles in galectin-1-mediated apoptosis of activated T-cells as well as progression of T-lymphoma. Previously, we demonstrated that $NF-{\kappa}B$ downregulated CD7 gene expression through the p38 MAPK pathway in developing immature thymocytes. However, its regulatory pathway is not well understood in functional mature T-cells. Here, we show that CD7 expression was downregulated by Twist2 in Jurkat cells, a human acute T-cell lymphoma cell line, and in EL4 cells, a mature murine T-cell lymphoma cell line. Furthermore, ectopic expression of Twist2 in Jurkat cells reduced galectin-1-induced apoptosis. While full-length Twist2 decreased CD7 promoter activity, a C-terminal deletion form of Twist2 reversed its inhibition, suggesting an important role of the C-terminus in CD7 regulation. In addition, CD7 expression was enhanced by histone deacetylase inhibitors such as trichostatin A and sodium butyrate, which indicates that Twist2 might be one of candidate factors involved in histone deacetylation. Based on these results, we conclude that upregulation of Twist2 increases the resistance to galectin-1-mediated-apoptosis, which may have significant implications for the progression of some T-cells into tumors such as Sezary cells.

Mesenchymal Stem Cells Ameliorate Fibrosis by Enhancing Autophagy via Inhibiting Galectin-3/Akt/mTOR Pathway and by Alleviating the EMT via Inhibiting Galectin-3/Akt/GSK3β/Snail Pathway in NRK-52E Fibrosis

  • Yu Zhao;Chuan Guo;Lianlin Zeng;Jialing Li;Xia Liu;Yiwei Wang;Kun Zhao;Bo Chen
    • International Journal of Stem Cells
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    • 제16권1호
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    • pp.52-65
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    • 2023
  • Background and Objectives: Epithelial-Mesenchymal transition (EMT) is one of the origins of myofibroblasts in renal interstitial fibrosis. Mesenchymal stem cells (MSCs) alleviating EMT has been proved, but the concrete mechanism is unclear. To explore the mechanism, serum-free MSCs conditioned medium (SF-MSCs-CM) was used to treat rat renal tubular epithelial cells (NRK-52E) fibrosis induced by transforming growth factor-β1 (TGF-β1) which ameliorated EMT. Methods and Results: Galectin-3 knockdown (Gal-3 KD) and overexpression (Gal-3 OE) lentiviral vectors were established and transfected into NRK-52E. NRK-52E fibrosis model was induced by TGF-β1 and treated with the SF-MSCs-CM for 24 h after modelling. Fibrosis and autophagy related indexes were detected by western blot and immunocytochemistry. In model group, the expressions of α-smooth muscle actin (α-SMA), fibronectin (FN), Galectin-3, Snail, Kim-1, and the ratios of P-Akt/Akt, P-GSK3β/GSK3β, P-PI3K/PI3K, P-mTOR/mTOR, TIMP1/MMP9, and LC3B-II/I were obviously increased, and E-Cadherin (E-cad) and P62 decreased significantly compared with control group. SF-MSCs-CM showed an opposite trend after treatment compared with model group. Whether in Gal-3 KD or Gal-3 OE NRK-52E cells, SF-MSCs-CM also showed similar trends. However, the effects of anti-fibrosis and enhanced autophagy in Gal-3 KD cells were more obvious than those in Gal-3 OE cells. Conclusions: SF-MSCs-CM probably alleviated the EMT via inhibiting Galectin-3/Akt/GSK3β/Snail pathway. Meanwhile, Gal-3 KD possibly enhanced autophagy via inhibiting Galectin-3/Akt/mTOR pathway, which synergistically ameliorated renal fibrosis. Targeting galectin-3 may be a potential target for the treatment of renal fibrosis.

Biophysical Feature, Crystallization and X-ray Crystallographic Studies of Toxascaris leonina Galectin

  • Sung, Min-Kyung;Jeong, Mi-Suk;Lee, Woo-Chul;Song, Jeong-Hyun;Kim, Hye-Yeon;Cho, Min-Kyoung;Yu, Hak-Sun;Jang, Se-Bok
    • Bulletin of the Korean Chemical Society
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    • 제33권1호
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    • pp.227-232
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    • 2012
  • Galectins are generally believed to be potential candidates for use in the development of novel antiinflammatory agents or as selective modulators of the immune response. In particular, galectin-9 exhibits some of the extracellular functions, including cell aggregation, adhesion, chemoattraction, activation, and apoptosis. Tl-galectin (Tl-gal, galectin-9 homologue gene) was isolated from an adult worm of the Toxascaris leonina. The full-length Tl-gal gene, which was incorporated into pET-28a, was overexpressed in E. coli and purified by nickel affinity and gel filtration chromatographies. The purified Tl-gal was crystallized using the hangingdrop vapor-diffusion method. The crystal belonged to the tetragonal space group $P4_1$, with unit-cell parameters of a = b = $75.7\AA$ and c = $248.4\AA$. The crystals were obtained at $20^{\circ}C$ and diffracted to a resolution of $3.0\AA$. The asymmetric unit contained four molecules of Tl-gal, which gave a crystal volume per protein mass (Vm) of $2.8\AA^3Da^{-1}$ and a solvent content of 54.1%.

Galectin-1 Promotes Gastric Carcinoma Progression and Cisplatin Resistance Through the NRP-1/c-JUN/Wee1 Pathway

  • Zhengyang Pan;Guoxi Xu;Yan Zhang;Meiling Wu;Jiahui Yu;Xujun He;Wei Zhang;Junfeng Hu
    • Journal of Gastric Cancer
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    • 제24권3호
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    • pp.300-315
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    • 2024
  • Purpose: Gastric cancer (GC) is among the deadliest malignancies and the third leading cause of cancer-related deaths worldwide. Galectin-1 (Gal-1) is a primary protein secreted by cancer-associated fibroblasts (CAFs); however, its role and mechanisms of action of Gal-1 in GC remain unclear. In this study, we stimulated GC cells with exogenous human recombinant galectin-1 protein (rhGal-1) to investigate its effects on the proliferation, migration, and resistance to cisplatin. Materials and Methods: We used simulated rhGal-1 protein as a paracrine factor produced by CAFs to induce GC cells and investigated its promotional effects and mechanisms in GC progression and cisplatin resistance. Immunohistochemical (IHC) assay confirmed that Gal-1 expression was associated with clinicopathological parameters and correlated with the expression of neuropilin-1 (NRP-1), c-JUN, and Wee1. Results: Our study reveals Gal-1 expression was significantly associated with poor outcomes. Gal-1 boosts the proliferation and metastasis of GC cells by activating the NRP-1/C-JUN/Wee1 pathway. Gal-1 notably increases GC cell resistance to cisplatin The NRP-1 inhibitor, EG00229, effectively counteracts these effects. Conclusions: These findings revealed a potential mechanism by which Gal-1 promotes GC growth and contributes to chemoresistance, offering new therapeutic targets for the treatment of GC.

Galectin-1 from redlip mullet Liza haematocheilia: identification, immune responses, and functional characterization as pattern recognition receptors (PRRs) in host immune defense system

  • Chaehyeon Lim;Hyukjae Kwon;Jehee Lee
    • Fisheries and Aquatic Sciences
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    • 제25권11호
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    • pp.559-571
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    • 2022
  • Galectins, a family of ß-galactoside-binding lectins, have emerged as soluble mediators in infected cells and pattern recognition receptors (PRRs) responsible for evoking and regulating innate immunity. The present study aimed to evaluate the role of galectin-1 in the host immune response of redlip mullet (Liza haematocheilia). We established a cDNA database for redlip mullet, and the cDNA sequence of galectin-1 (LhGal-1) was characterized. In silico analysis was performed, and the spatial and temporal expression patterns in gills and blood in response to lipopolysaccharide polyinosinic:polycytidylic acid, and Lactococcus garvieae were estimated via quantitative real-time PCR. Functional assays were conducted using recombinant protein to investigate carbohydrate binding, bacterial binding, and bacterial agglutination activity. LhGal-1 was composed of 135 amino acids. Conserved motifs (H-NPR, -N- and -W-E-R) within the carbohydrate recognition domain were found in LhGal-1. The tissue distribution revealed that the healthy stomach expressed high levels of LhGal-1. The temporal monitoring of LhGal-1 mRNA expression in the gill and blood showed its significant upregulation in response to immune challenges with different stimulants. rLhGal-1 exhibited binding activity in response to carbohydrates and bacteria. Moreover, the agglutination of rLhGal-1 against Escherichia coli was observed. Collectively, our findings suggest that LhGal-1 may function as a PRR in redlip mullet. Furthermore, LhGal-1 can be considered a significant gene to play a protective role in redlip mullet immune system.

소포성 갑상샘 유두암종의 세침흡인 세포검사의 정확도와 Galectin-3 면역염색의 유용성 (The Diagnostic Accuracy of Fine Needle Aspiration Cytology and the Diagnostic Usefulness of Galectin-3 Immunostaining for the Follicular Variant of Papillary Thyroid Carcinoma)

  • 정찬권;신정하;이현승;이아원;정은선;최영진;이교영
    • 대한세포병리학회지
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    • 제19권2호
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    • pp.160-163
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    • 2008
  • The cytologic diagnosis of the follicular variant of papillary thyroid carcinoma (FVPTC) has become one of the common causes of false negative diagnoses when performing fine needle aspiration cytology (FNAC) of the thyroid gland. We retrospectively reviewed all the aspirates for which a diagnosis of FVPTC had been made based on the surgically excised specimens, regardless of the cytologic diagnosis. 145 FNACs was performed in 135 patients. The cytologic diagnoses were categorized as 2 unsatisfactory specimens (1.4%), 16 benign (11.0%), 49 atypical (33.8%) and 78 malignant lesions (53.8%). The tumor cells consistently showed significant nuclear overlapping, irregular nuclei and fine chromatin in all cases; however, nuclear grooves and inclusions were scarce. Galectin-3 immunostaining was performed on the cell blocks of 65 cases and this was positive for 45 cases (69.2%). The results of our study demonstrate that the determination of minimal cytologic criteria is needed to raise the sensitivity of detecting FVPTC by FNAC, and galectin-3 immunostaining is useful to make decisions on the surgical treatment of cytologically atypical thyroid nodules.

Histopathological evaluation of the lungs in experimental autoimmune encephalomyelitis

  • Sungmoo Hong;Jeongtae Kim;Kyungsook Jung;Meejung Ahn;Changjong Moon;Yoshihiro Nomura;Hiroshi Matsuda;Akane Tanaka;Hyohoon Jeong;Taekyun Shin
    • Journal of Veterinary Science
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    • 제25권3호
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    • pp.35.1-35.13
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    • 2024
  • Importance: Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis characterized by inflammation within the central nervous system. However, inflammation in non-neuronal tissues, including the lungs, has not been fully evaluated. Objective: This study evaluated the inflammatory response in lungs of EAE mice by immunohistochemistry and histochemistry. Methods: Eight adult C57BL/6 mice were injected with myelin oligodendrocyte glycoprotein35-55 to induce the EAE. Lungs and spinal cords were sampled from the experimental mice at the time of sacrifice and used for the western blotting, histochemistry, and immunohistochemistry. Results: Histopathological examination revealed inflammatory lesions in the lungs of EAE mice, characterized by infiltration of myeloperoxidase (MPO)- and galectin-3-positive cells, as determined by immunohistochemistry. Increased numbers of collagen fibers in the lungs of EAE mice were confirmed by histopathological analysis. Western blotting revealed significantly elevated level of osteopontin (OPN), cluster of differentiation 44 (CD44), MPO and galectin-3 in the lungs of EAE mice compared with normal controls (p < 0.05). Immunohistochemical analysis revealed both OPN and CD44 in ionized calcium-binding adapter molecule 1-positive macrophages within the lungs of EAE mice. Conclusions and Relevance: Taken together, these findings suggest that the increased OPN level in lungs of EAE mice led to inflammation; concurrent increases in proinflammatory factors (OPN and galectin-3) caused pulmonary impairment.