The functional spectrum of human galectins is currently explored, with a wide range of activities being described. The role of galectin-3 as adhesin for bacteria is based on its strong binding to lipopolysaccharides (LPSs), which brings the possibility of such a contamination in galectin preparations to awareness. This assumption was verified in three independent functional assay systems using polymyxin B as inhibitor of LPS-dependent effects. Moreover, a commercial LPS quantification kit also revealed LPS in galectin preparations. Chromatography was effective in removing LPS, suggesting that such a technique needs to be applied to prevent assigning cellular responses to galectins rather than LPS.
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http://dx.doi.org/10.1016/j.bbrc.2008.12.024 | DOI Listing |
Angew Chem Int Ed Engl
January 2025
Department of Chemistry and Center for Diagnostics & Therapeutics, Georgia State University, 50 Decatur Street SE, Atlanta, GA 30303, USA.
Poly-N-acetyllactosamine (poly-LacNAc) is ubiquitously expressed on cell surface glycoconjugates, serving as the backbone of complex glycans and an extended scaffold that presents diverse glycan epitopes. The branching of poly-LacNAc, where internal galactose (Gal) residues have β1-6 linked N-acetylglucosamine (GlcNAc) attached, forms the blood group I-antigen, which is closely associated with various physiological and pathological processes including cancer progression. However, the underlying mechanisms remain unclear as many of the I-antigen sequences are undefined and inaccessible.
View Article and Find Full Text PDFBioact Mater
December 2024
Center for Biomaterials, Biomedical Research Institute, Korea Institute of Science and Technology (KIST), Hwarangno 14-gil 5, Seongbuk-gu, Seoul, 02792, Republic of Korea.
Modulating inflammatory cells in an implantation site leads to severe complications and still unsolved challenges for blood-contacting medical devices. Inspired by the role of galectin-1 (Gal-1) in selective functions on multiple cells and immunomodulatory processes, we prepared a biologically target-specific surface coated with the lipid bilayer containing Gal-1 (Gal-1-SLB) and investigate the proof of the biological effects. First, lipoamido-dPEG-acid was deposited on a gold-coated substrate to form a self-assembled monolayer and then conjugated dioleoylphosphatidylethanolamine (DOPE) onto that to produce a lower leaflet of the supported lipid bilayer (SLB) before fusing membrane-derived vesicles extracted from B16-F10 cells.
View Article and Find Full Text PDFInt Immunopharmacol
November 2024
Department of General Practice, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325027, China; Wenzhou Key Laboratory of Precision General Practice and Health Management, Wenzhou 325000, China; South Zhejiang Institute of Radiation Medicine and Nuclear Technology, Wenzhou 325014, China; Department of General Practice, Taizhou Women and Children's Hospital of Wenzhou Medical University, Taizhou 318001, China. Electronic address:
Pulmonary fibrosis (PF) results from excessive extracellular matrix (ECM) deposition and tissue remodeling after activation of fibroblasts into myofibroblasts. Abnormally deposited fibrotic ECM, in turn, promotes fibroblast activation and accelerates loss of lung structure and function. However, the molecular mediators and exact mechanisms by which fibrotic ECM promotes fibroblast activation are unclear.
View Article and Find Full Text PDFCurr Top Med Chem
October 2024
School of Dentistry and Medical Sciences, Charles Sturt University, Orange, NSW, Australia.
Eur J Pharm Sci
June 2024
Department of Pharmaceutics, Key Laboratory of Chemical Biology of Ministry of Education, School of Pharmaceutical Sciences, Cheelloo College of Medicine, Shandong University, 44 West Wenhua Road, Jinan, Shandong 250012, China; Key University Laboratory of Pharmaceutics & Drug Delivery Systems of Shandong Province, School of Pharmaceutical Sciences, Cheeloo College of Medicine, Shandong University, 44 West Wenhua Road, Jinan, Shandong 250012, China; Pediatric Pharmaceutical Engineering Laboratory of Shandong Province, Shandong Dyne Marine Biopharmaceutical Company Limited, Rongcheng, Shandong 264300, China; Chemical Immunopharmaceutical Engineering Laboratory of Shandong Province, Shandong Xili Pharmaceutical Company Limited, Heze, Shandong 274300, China. Electronic address:
Orally marketed products nintedanib (NDNB) and pirfenidone (PFD) for pulmonary fibrosis (PF) are administered in high doses and have been shown to have serious toxic and side effects. NDNB can cause the elevation of galectin-3, which activates the NF-κB signaling pathway and causes the inflammatory response. S-allylmercapto-N-acetylcysteine (ASSNAC) can alleviate the inflammation response by inhibiting the TLR-4/NF-κB signaling pathway.
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