ArticleAmerican journal of physiology. Cell physiology2013
Identification of a high-mannose ICAM-1 glycoform: effects of ICAM-1 hypoglycosylation on monocyte adhesion and outside in signaling.
Article in American journal of physiology. Cell physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 59 citations in OpenAlex.
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- Elevated neuraminidase potentiates lung inflammation through facilitating integrin β2-mediated adhesion and immune responses of neutrophils.The Journal of biological chemistry · 2026Article
- Genome-wide CRISPR/Cas9 screen reveals factors that influence the susceptibility of tumor cells to NK cell-mediated killing.Journal for immunotherapy of cancer · 2025Article
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- Alterations of mannosylated glycopatterns recognized by Hippeastrum hybrid lectin in saliva of patients with lung cancer.Clinical oral investigations · 2024Article
- Structure-Activity Relationship of Oleanane-Type Pentacyclic Triterpenoids on Nuclear Factor κB Activation and Intracellular Trafficking andInternational journal of molecular sciences · 2024Article
- Iron regulates the quiescence of naive CD4 T cells by controlling mitochondria and cellular metabolism.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
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- Revisiting the immunopathology of congenital disorders of glycosylation: an updated review.Frontiers in immunology · 2024Review
- The crosstalk between neuropilin-1 and tumor necrosis factor-α in endothelial cells.Frontiers in cell and developmental biology · 2024Article
- NADPH Oxidase 4-mediated Alveolar Macrophage Recruitment to Lung Attenuates Neutrophilic Inflammation inImmune network · 2023Article
- Review
- Endothelial transmigration hotspots limit vascular leakage through heterogeneous expression of ICAM-1.EMBO reports · 2023Article
- Large-scale expansion of human umbilical cord-derived mesenchymal stem cells using PLGA@PLL scaffold.Bioresources and bioprocessing · 2023Article
- A role for endothelial alpha-mannosidase MAN1C1 in radiation-induced immune cell recruitment.iScience · 2022Article
- Bioactive Evaluation of Ursane-Type Pentacyclic Triterpenoids:Molecules (Basel, Switzerland) · 2022Article
- N-Glycosylation and Inflammation; the Not-So-Sweet Relation.Frontiers in immunology · 2022Review
- Clinical importance of high-mannose, fucosylated, and complex N-glycans in breast cancer metastasis.JCI insight · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Endothelial adhesion molecules are critical effectors of inflammation ensuring coordinated interactions that allow leukocytes to home to sites of injury. These adhesion molecules are often extensively modified posttranslationaly by the addition of N-glycans, but if, or how, these modifications contribute to the protein function remains poorly understood. Herein we show that activated endothelial cells express two distinct N-glycoforms of intercellular adhesion molecule 1 (ICAM-1) that comprise a complex N-glycoform with α-2,6 sialic acid present at relatively high levels and a second, less abundant and previously undescribed high-mannose glycoform (HM-ICAM-1). This novel HM-ICAM-1 glycoform was also detected in human coronary artery specimens and moreover appeared to be the dominant glycoform in vivo. Production of exclusively HM-ICAM-1 in cells by α-mannosidase inhibition increased monocyte rolling and adhesion compared with mature ICAM-1 consistent with high-mannose epitopes providing leukocyte ligands. Cross-linking of ICAM-1 transmits outside-in signals that affect endothelial permeability and survival. Interestingly, cell signaling (assessed using ERK, VE-cadherin, and Akt phosphorylation) was maintained after cross-linking of HM-ICAM-1 compared with mature ICAM-1; however, interactions with the actin cytoskeleton were lost with HM-ICAM-1. These findings suggest that specific ICAM-1 N-glycoforms modulate distinct aspects of the inflammatory response and identify HM-ICAM-1 as a new therapeutic target for controlling leukocyte trafficking and endothelial inflammation.
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