Correction to: Matrix metalloproteinase 9 induces endothelial-mesenchymal transition via Notch activation in human kidney glomerular endothelial cells
| العنوان: | Correction to: Matrix metalloproteinase 9 induces endothelial-mesenchymal transition via Notch activation in human kidney glomerular endothelial cells |
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| المؤلفون: | Hong Zhao, Tian Kui Tan, David Harris, Stephen I. Alexander, Guoping Zheng, Yun Zhang, Ya Wang, Padmashree Rao, Yuan Min Wang, Qi Cao, Jianlin Zhang, Yiping Wang, Ye Zhao, Vincent W. Lee, Lihua Wang, Xi Qiao |
| المصدر: | BMC Molecular and Cell Biology BMC Molecular and Cell Biology, Vol 21, Iss 1, Pp 1-1 (2020) |
| بيانات النشر: | BioMed Central, 2020. |
| سنة النشر: | 2020 |
| مصطلحات موضوعية: | Transition (genetics), Receptors, Notch, Chemistry, lcsh:Cytology, Mesenchymal stem cell, Kidney Glomerulus, Correction, Endothelial Cells, Matrix metalloproteinase 9, Human kidney, Cell Biology, Dipeptides, Matrix Metalloproteinase Inhibitors, Recombinant Proteins, Mesoderm, Transforming Growth Factor beta1, Matrix Metalloproteinase 9, Cancer research, Humans, lcsh:QH573-671, Amyloid Precursor Protein Secretases, Molecular Biology, Signal Transduction |
| الوصف: | Endothelial-mesenchymal transition (EndoMT) is a major source of myofibroblast formation in kidney fibrosis. Our previous study showed a profibrotic role for matrix metalloproteinase 9 (MMP-9) in kidney fibrosis via induction of epithelial-mesenchymal transition (EMT). Inhibition of MMP-9 activity reduced kidney fibrosis in murine unilateral ureteral obstruction. This study investigated whether MMP-9 also plays a role in EndoMT in human glomerular endothelial cells.TGF-β1 (10 or 20 ng/ml) induced EndoMT in HKGECs as shown by morphological changes. In addition, VE-cadherin and CD31 were significantly downregulated, whereas α-SMA, vimentin, and N-cadherin were upregulated. RT-PCR revealed that Snail, a known inducer of EMT, was upregulated. The MMP inhibitor GM6001 abrogated TGF-β1-induced EndoMT. Zymography indicated that MMP-9 was also upregulated in TGF-β1-treated HKGECs. Recombinant MMP-9 (2 μg/ml) induced EndoMT in HKGECs via Notch signaling, as evidenced by increased formation of the Notch intracellular domain (NICD) and decreased Notch 1. Inhibition of MMP-9 activity by its inhibitor showed a dose-dependent response in preventing TGF-β1-induced α-SMA and NICD in HKGECs, whereas inhibition of Notch signaling by γ-secretase inhibitor (GSI) blocked rMMP-9-induced EndoMT.Taken together, our results demonstrate that MMP-9 plays an important role in TGF-β1-induced EndoMT via upregulation of Notch signaling in HKGECs. |
| اللغة: | English |
| تدمد: | 2661-8850 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6527dfb4601bdcf39fa0afff81097547 http://europepmc.org/articles/PMC7576858 |
| حقوق: | OPEN |
| رقم الأكسشن: | edsair.doi.dedup.....6527dfb4601bdcf39fa0afff81097547 |
| قاعدة البيانات: | OpenAIRE |
Find this article in full text from Springer Verlag. | تدمد: | 26618850 |
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