ArticleBiology open2019
Discoidin domain receptor 1 deficiency in vascular smooth muscle cells leads to mislocalisation of N-cadherin contacts.
Article in Biology open, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Discoidin domain receptor 1 (DDR1): An emerged novel mechanosensor.Fundamental research · 2026Review
- Endothelial discoidin domain receptor 1 senses flow to modulate YAP activation.Nature communications · 2023Article
- Receptor Tyrosine Kinase: Still an Interesting Target to Inhibit the Proliferation of Vascular Smooth Muscle Cells.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2023Review
- Silencing of sinusoidal DDR1 reduces murine liver metastasis by colon carcinoma.Scientific reports · 2020Article
- DDR1 (Discoidin Domain Receptor-1)-RhoA (Ras Homolog Family Member A) Axis Senses Matrix Stiffness to Promote Vascular Calcification.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N-cadherin mediates cell-cell contacts in vascular smooth muscle cells (VSMCs), and regulates VSMC behaviours including migration and proliferation. Discoidin domain receptor 1 (DDR1) is a collagen binding receptor also implicated in these processes. Previous studies have shown that both N-cadherin and DDR1 are upregulated after vascular injury, but it is not known whether there is a relationship between the two molecules. In the current study we found that N-cadherin was mislocalised from cell-cell junctions in the absence of DDR1. This occurred in spite of the fact that there was no significant difference in total cell lysate levels of N-cadherin between DDR1+/+ and DDR1-/- VSMCs. Analysis of lipid raft fractions revealed decreased N-cadherin and associated junctional complex catenins in DDR1-/- compared to DDR1+/+ VSMCs. Treatment with cholesterol oxidase or methyl-β-cyclodextrin to disrupt lipid rafts removed N-cadherin and DDR1 from the raft fractions. Reciprocal co-immunoprecipitations suggested the association of DDR1 and N-cadherin. Importantly, transfection of DDR1-/- cells with full-length DDR1b rescued the formation of N-cadherin junctions. Together, these data reveal that N-cadherin cell-cell contacts in VSMCs are regulated through interactions with DDR1 and both molecules are located in lipid rafts.
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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.