Discoidin domain receptor 1 deficiency in vascular smooth muscle cells leads to mislocalisation of N-cadherin contacts

Biology Open
Songyi XuMichelle P Bendeck

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 r...Continue Reading

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Citations

Jun 5, 2020·Arteriosclerosis, Thrombosis, and Vascular Biology·David NgaiMichelle P Bendeck
Oct 29, 2020·Scientific Reports·Irene RomayorElvira Olaso
Mar 25, 2021·Mathematical Biosciences and Engineering : MBE·Guoyi KeWenrui Hao

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Datasets Mentioned

BETA
GM1

Methods Mentioned

BETA
co-immunoprecipitation
co-immunoprecipitations
Immunoprecipitation
transfection
GTPases
scraping

Software Mentioned

ImageJ

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