ArticleBioengineering & translational medicine2017
ICAM-1-Targeted Nanocarriers Attenuate Endothelial Release of Soluble ICAM-1, an Inflammatory Regulator.
Article in Bioengineering & translational medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The trial behind it
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Application of nanotherapy in cardiovascular diseases featuring novel pharmacological mechanisms and drug delivery strategies.Discover nano · 2026Review
- ICAM-1 targeting of nanocarriers in a human blood-brain-barrier-on-a-chip complementsJournal of drug targeting · 2026Article
- Application of an intercellular adhesion molecule-1-targeted nanoparticles loaded with irisin in postoperative neurocognitive disorder through metabolic axis activation and barrier restoration.Journal of nanobiotechnology · 2026Article
- Endothelial Glycocalyx Turnover in Vascular Health and Disease: Rethinking Endothelial Dysfunction.Annual review of biochemistry · 2025Review
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- Poly(lactic-co-glycolic acid) nanoparticle fabrication, functionalization, and biological considerations for drug delivery.Biomicrofluidics · 2024Review
- Article
- Combination of Physicochemical Tropism and Affinity Moiety Targeting of Lipid Nanoparticles Enhances Organ Targeting.Nano letters · 2024Article
- Protein Corona Attenuates the Targeting of Antitumor Sialyl Lewis X-Decorated Liposomes to Vascular Endothelial Cells under Flow Conditions.Pharmaceutics · 2023Article
- Nanobiotechnology approaches for cardiovascular diseases: site-specific targeting of drugs and nanoparticles for atherothrombosis.Journal of nanobiotechnology · 2022Review
- Recent Advances in the Surface Functionalization of PLGA-Based Nanomedicines.Nanomaterials (Basel, Switzerland) · 2022Review
- Targeting pulmonary vascular endothelial cells for the treatment of respiratory diseases.Frontiers in pharmacology · 2022Review
- New Approaches in Nanomedicine for Ischemic Stroke.Pharmaceutics · 2021Review
- Intertwined mechanisms define transport of anti-ICAM nanocarriers across the endothelium and brain delivery of a therapeutic enzyme.Journal of controlled release : official journal of the Controlled Release Society · 2020Article
- Editorial: The launch phase ofBioengineering & translational medicine · 2019Article
- Induction of osteoclast-like cell formation by leptin-induced soluble intercellular adhesion molecule secreted from cancer cells.Therapeutic advances in medical oncology · 2019Article
- Review
- Lysosomal enzyme replacement therapies: Historical development, clinical outcomes, and future perspectives.Advanced drug delivery reviews · 2017Review
- Introduction to special issue: Bioengineered Therapeutics. The Next Generation of Drug Development.Bioengineering & translational medicine · 2017Article
- ICAM-1 targeting, intracellular trafficking, and functional activity of polymer nanocarriers coated with a fibrinogen-derived peptide for lysosomal enzyme replacement.Journal of drug targetingArticle
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Targeting of drug nanocarriers (NCs) to intercellular adhesion molecule-1 (ICAM-1), an endothelial-surface protein overexpressed in many pathologies, has shown promise for therapeutic delivery into and across this lining. Yet, due to the role of ICAM-1 in inflammation, the effects of targeting this receptor need investigation. Since ICAM-1 binding by natural ligands (leukocyte integrins) results in release of the "soluble ICAM-1" ectodomain (sICAM-1), an inflammatory regulator, we investigated the influence of targeting ICAM-1 with NCs on this process. For this, sICAM-1 was measured by ELISA from cell-medium supernatants, after incubation of endothelial cell (EC) monolayers in the absence versus presence of anti-ICAM NCs. In the absence of NCs, ECs released sICAM-1 when treated with a pro-inflammatory cytokine (TNFα). This was reduced by inhibiting matrix metalloproteinases MMP-9 or MMP-2, yet inhibiting both did not render additive effects. Release of sICAM-1 mainly occurred at the basolateral versus apical side, and both MMP-9 and MMP-2 influenced apical release, while basolateral release depended on MMP-9. Interestingly, anti-ICAM NCs reduced sICAM-1 to a greater extent than MMP inhibition, both at the apical and basolateral sides. This effect was enhanced with time, although NCs had been removed after binding to cells, ruling out a "trapping" effect of NCs. Instead, inhibiting anti-ICAM NC endocytosis counteracted their inhibition on sICAM-1 release. Hence, anti-ICAM NCs inhibited sICAM-1 release by mobilizing ICAM-1 from the cell-surface into intracellular vesicles. Since elevated levels of sICAM-1 associate with numerous diseases, this effect represents a secondary benefit of using ICAM-1-targeted NCs for drug delivery.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.