PSGL-1, the optimal selectin ligand demonstrated by in vivo studies to date, is an essential adhesive molecule mediating the rolling of leukocytes on the endothelial cells and the recruitment of leukocytes to the inflamed tissue. Recent studies demonstrated, in addition to its direct role in capture of leukocytes from the bloodstream, PSGL-1 also functions as a signal-transducing receptor and initiates a series of intracellular signal events during the activation of leukocytes. Our present work showed antibody engagement of PSGL-1 upregulated the transcriptional activity of CSF-1 promotor and increased the endogenous expression of CSF-1 mRNA in Jurkat cell. Overexpression of wild-typed non-receptor tyrosine kinase Syk, but not kinase dead mutant of Syk, promoted the upregulation of the transcriptional activity of CSF-1 promoter caused by antibody engagement of PSGL-1. Additionally, special inhibitor of Syk Piceatannol suppressed the increase of CSF-1 mRNA caused by the engagement of PSGL-1. The results suggest that signal transducted by PSGL-1 upregulate the transcriptional activity of CSF-1, and non-receptor tyrosine kinase Syk participates in this pathway.
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Early results indicate that de-O-acetylated sialic acids increase Selectin binding in cancers.
Front Oncol
December 2024
Department of Chemistry, Biochemistry and Physics, South Dakota State University, Brookings, SD, United States.
Cancers utilize a simple glycan, Sialic Acid, to engage in metastatic processes via the Sialic acid (Sia) -Selectin pathway. Selectins recognize and bind to sialylated substrates, resulting in adhesion, migration, and extravasation, however, how deviations from the canonical form of Sia regulate binding to Selectin receptors (E, L, and P) on hemopoietic cells resulting in these metastatic processes, remained a gap in knowledge. De-O-acetylated Sias has been recently shown to be an integral substrate to the binding of sialic acid binding proteins.
View Article and Find Full Text PDFPSGL-1 decorated with sialyl Lewis promotes high affinity binding of myeloma cells to P-selectin but is dispensable for E-selectin engagement.
Sci Rep
January 2024
Hematology, Department of Translational and Precision Medicine, Sapienza University, Rome, Italy.
Dissemination of multiple myeloma into the bone marrow proceeds through sequential steps mediated by a variety of adhesion molecules and chemokines that eventually results in the extravasation of malignant plasma cells into this protective niche. Selectins are a class of C-type lectins that recognize carbohydrate structures exposed on blood borne cells and participate in the first step of the extravasation cascade, serving as brakes to slow down circulating cells enabling them to establish firm adhesion onto the endothelium. Myeloma cells enriched for the expression of selectin ligands present an aggressive disease in vivo that is refractory to bortezomib treatment and can be reverted by small molecules targeting E-selectin.
View Article and Find Full Text PDFHow E-, L-, and P-Selectins Bind to sLe and PSGL-1: A Quantification of Critical Residue Interactions.
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Institute of Chemistry, SAS, Dubravska cesta 9, 84538 Bratislava, Slovakia.
Selectins and their ability to interact with specific ligands are a cornerstone in cell communication. Over the last three decades, a considerable wealth of experimental and molecular modeling insights into their structure and were gathered. Nonetheless, explaining the role of individual selectin residues on a quantitative level remained elusive, despite its importance in understanding the structure-function relationship in these molecules and designing their inhibitors.
View Article and Find Full Text PDFATRA treatment slowed P-selectin-mediated rolling of flowing HL60 cells in a mechano-chemical-dependent manner.
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Institute of Mechanics/School of Biology and Biological Engineering, South China University of Technology, Guangzhou, China.
Article Synopsis
- ATRA induces differentiation of acute promyelocytic leukemia (APL) cells into granulocytes, potentially leading to differentiation syndrome (DS), with limited understanding of the mechano-chemical regulation involved in this process.
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- Mechanistically, ATRA treatment increased adhesion through faster activation of β2 integrins and elevated expression of adhesion molecules, suggesting a new therapeutic approach for managing APL differentiation syndrome by targeting these adhesion factors.
B-cell receptor associated protein 31 deficiency decreases the expression of adhesion molecule CD11b/CD18 and PSGL-1 in neutrophils to ameliorate acute lung injury.
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November 2022
Institute of Biochemistry and Molecular Biology, College of Life and Health Sciences, Northeastern University, Shenyang 110819, China. Electronic address:
Acute lung injury (ALI) and its more severe condition acute respiratory distress syndrome (ARDS) are critical life-threatening disorders characterized by an excessive influx of neutrophils into the alveolar space. Neutrophil infiltration is a multi-step process involving the sequential engagement of adhesion molecules. The adhesion molecule CD11b/CD18 acts as an important role in the recruitment of neutrophils to lung tissues in the ALI model.
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