miR-126 Is Involved in Vascular Remodeling under Laminar Shear Stress
Autor: | Hanna Hlawaty, Eléonore M'Baya-Moutoula, Valérie Metzinger-Le Meuth, Ziad A. Massy, Laurent Metzinger, Nathalie Charnaux, Fatiha Taïbi, Ana Mondadori dos Santos, Oualid Haddad |
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Jazyk: | angličtina |
Rok vydání: | 2015 |
Předmět: |
Receptors
CXCR4 Stromal cell Article Subject Kruppel-Like Transcription Factors Vascular Cell Adhesion Molecule-1 lcsh:Medicine Inflammation Apoptosis Biology Vascular Remodeling Models Biological General Biochemistry Genetics and Molecular Biology Apolipoproteins E Downregulation and upregulation Gene expression medicine Human Umbilical Vein Endothelial Cells Animals Humans RNA Messenger Cell Shape Cell Proliferation Regulation of gene expression Mice Knockout General Immunology and Microbiology Cell growth Cell adhesion molecule lcsh:R General Medicine Actins Chemokine CXCL12 Cell biology Mice Inbred C57BL MicroRNAs Gene Expression Regulation embryonic structures cardiovascular system Female Syndecan-4 Stress Mechanical Syndecan-1 medicine.symptom RGS Proteins Research Article |
Zdroj: | BioMed Research International, Vol 2015 (2015) BioMed Research International |
ISSN: | 2314-6141 2314-6133 |
Popis: | Morphology and changes in gene expression of vascular endothelium are mainly due to shear stress and inflammation. Cell phenotype modulation has been clearly demonstrated to be controlled by small noncoding micro-RNAs (miRNAs). This study focused on the effect of laminar shear stress (LSS) on human endothelial cells (HUVECs), with an emphasis on the role of miRNA-126 (miR-126). Exposure of HUVECsin vitroto LSS modified the shape of HUVECs and concomitantly regulated the expression of miR-126, vascular cell adhesion molecule 1 (VCAM-1), and syndecan-4 (SDC-4). A significant upregulation of miR-126 during long-term exposure to flow was shown. Interestingly, LSS enhanced SDC-4 expression on the HUVEC membranes. Overexpression of miR-126 in HUVECs decreased the levels of targets stromal cell-derived factor-1 SDF-1/CXCL12 and VCAM-1 but increased the expression of RGS16, CXCR4, and SDC-4. No significant difference in terms of cell proliferation and apoptosis was observed between scramble, anti-miR-126, and pre-miR-126 transfected HUVECs. In Apo-E KO/CKD mice aortas expressing a high level of miR-126, SDC-4 was concomitantly increased. In conclusion, our results suggest that miR-126 (i) is overexpressed by long-term LSS, (ii) has a role in up- and downregulation of genes involved in atherosclerosis, and (iii) affects SDC-4 expression. |
Databáze: | OpenAIRE |
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