Epithelial–mesenchymal status influences how cells deposit fibrillin microfibrils

Baldwin, Andrew K. ORCID: 0000-0002-8331-6769, Cain, Stuart Alan, Lennon, Rachel, Godwin, Alan, Merry, Catherine L. R. and Kielty, Cay M. (2014) Epithelial–mesenchymal status influences how cells deposit fibrillin microfibrils. Journal of Cell Science, 127. pp. 158-171. ISSN 0021-9533

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Abstract

Here, we show that epithelial–mesenchymal status influences how cells deposit extracellular matrix. Retinal pigmented epithelial (RPE) cells that expressed high levels of E-cadherin and had cell–cell junctions rich in zona occludens (ZO)-1, b-catenin and heparan sulfate, required syndecan-4 but not fibronectin or protein kinase C a (PKCa) to assemble extracellular matrix (fibrillin microfibrils and perlecan). In contrast, RPE cells that strongly expressed mesenchymal smooth muscle a-actin but little ZO-1 or E-cadherin, required fibronectin (like fibroblasts) and PKCa, but not syndecan-4. Integrins a5b1 and/or a8b1 and actomyosin tension were common requirements for microfibril deposition, as was heparan sulfate biosynthesis. TGFb, which stimulates epithelial–mesenchymal transition, altered gene expression and overcame the dependency on syndecan-4 for microfibril deposition in epithelial RPE cells, whereas blocking cadherin interactions disrupted microfibril deposition. Renal podocytes had a transitional phenotype with pericellular b-catenin but little ZO-1; they required syndecan-4 and fibronectin for efficient microfibril deposition. Thus, epithelial–mesenchymal status modulates microfibril deposition.

Item Type: Article
Uncontrolled Keywords: Epithelial cell, Mesenchymal cell, Fibrillin-1, Fibronectin, Perlecan, Integrin, Syndecan, Cell–cell junction
Subjects: Q Science > QR Microbiology
Divisions: ?? biology ??
Depositing User: Sarah Taylor
Date Deposited: 01 Mar 2018 09:05
Last Modified: 01 Mar 2018 09:05
Identification Number: 10.1242/jcs.134270
URI: http://ubir.bolton.ac.uk/id/eprint/1385

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