ArticleThe Journal of biological chemistry2019
The cell adhesion molecule IGPR-1 is activated by and regulates responses of endothelial cells to shear stress.
Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
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- Low Intraocular Pressure Induces Fibrotic Changes in the Trabecular Meshwork and Schlemm's Canal of Sprague Dawley Rats.Translational vision science & technology · 2024Article
- Low or oscillatory shear stress and endothelial permeability in atherosclerosis.Frontiers in physiology · 2024Review
- Oscillatory shear stress-induced downregulation of TET1s injures vascular endothelial planar cell polarity by suppression of actin polymerization.APL bioengineering · 2023Article
- Article
- Adhesion to the Brain Endothelium Selects Breast Cancer Cells with Brain Metastasis Potential.International journal of molecular sciences · 2023Article
- The role of NEDD4 related HECT-type E3 ubiquitin ligases in defective autophagy in cancer cells: molecular mechanisms and therapeutic perspectives.Molecular medicine (Cambridge, Mass.) · 2023Review
- Different hemodynamic factors cause the occurrence of superior mesenteric atherosclerotic stenosis and superior mesenteric artery dissection.Frontiers in cardiovascular medicine · 2023Article
- Human endogenous retrovirus-H long terminal repeat-associating 2: The next immune checkpoint for antitumour therapy.EBioMedicine · 2022Review
- The cell adhesion molecule TMIGD1 binds to moesin and regulates tubulin acetylation and cell migration.Journal of biomedical science · 2021Article
- A functional outside-in signaling network of proteoglycans and matrix molecules regulating autophagy.Matrix biology : journal of the International Society for Matrix Biology · 2021Article
- NEDD4 regulates ubiquitination and stability of the cell adhesion molecule IGPR-1 via lysosomal pathway.Journal of biomedical science · 2021Article
- AMP-activated protein kinase is a key regulator of acute neurovascular permeability.Journal of cell science · 2021Article
- Cell adhesion molecule IGPR-1 activates AMPK connecting cell adhesion to autophagy.The Journal of biological chemistry · 2020Article
- Current understanding of intimal hyperplasia and effect of compliance in synthetic small diameter vascular grafts.Biomaterials science · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Vascular endothelial cells respond to blood flow-induced shear stress. However, the mechanisms through which endothelial cells transduce mechanical signals to cellular responses remain poorly understood. In this report, using tensile-force assays, immunofluorescence and atomic force microscopy, we demonstrate that immunoglobulin and proline-rich receptor-1 (IGPR-1) responds to mechanical stimulation and increases the stiffness of endothelial cells. We observed that IGPR-1 is activated by shear stress and tensile force and that flow shear stress-mediated IGPR-1 activation modulates remodeling of endothelial cells. We found that under static conditions, IGPR-1 is present at the cell-cell contacts; however, under shear stress, it redistributes along the cell borders into the flow direction. IGPR-1 activation stimulated actin stress fiber assembly and cross-linking with vinculin. Moreover, we noted that IGPR-1 stabilizes cell-cell junctions of endothelial cells as determined by staining of cells with ZO1. Mechanistically, shear stress stimulated activation of AKT Ser/Thr kinase 1 (AKT1), leading to phosphorylation of IGPR-1 at Ser-220. Inhibition of this phosphorylation prevented shear stress-induced actin fiber assembly and endothelial cell remodeling. Our findings indicate that IGPR-1 is an important player in endothelial cell mechanosensing, insights that have important implications for the pathogenesis of common maladies, including ischemic heart diseases and inflammation.
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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.