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MiR-126-3p Is Dynamically Regulated in Endothelial-to-Mesenchymal Transition during Fibrosis.

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Title: MiR-126-3p Is Dynamically Regulated in Endothelial-to-Mesenchymal Transition during Fibrosis.
Authors: Jordan, Nina P., Tingle, Samuel J., Shuttleworth, Victoria G., Cooke, Katie, Redgrave, Rachael E., Singh, Esha, Glover, Emily K., Ahmad Tajuddin, Hafiza B., Kirby, John A., Arthur, Helen M., Ward, Chris, Sheerin, Neil S., Ali, Simi
Source: International Journal of Molecular Sciences; Aug2021, Vol. 22 Issue 16, p8629-8629, 1p
Subject Terms: RENAL fibrosis, FIBROSIS, RENAL biopsy, HEART fibrosis, HEART injuries, ENDOTHELIAL cells
Abstract: In fibrotic diseases, myofibroblasts derive from a range of cell types including endothelial-to-mesenchymal transition (EndMT). Increasing evidence suggests that miRNAs are key regulators in biological processes but their profile is relatively understudied in EndMT. In human umbilical vein endothelial cells (HUVEC), EndMT was induced by treatment with TGFβ2 and IL1β. A significant decrease in endothelial markers such as VE-cadherin, CD31 and an increase in mesenchymal markers such as fibronectin were observed. In parallel, miRNA profiling showed that miR-126-3p was down-regulated in HUVECs undergoing EndMT and over-expression of miR-126-3p prevented EndMT, maintaining CD31 and repressing fibronectin expression. EndMT was investigated using lineage tracing with transgenic Cdh5-Cre-ERT2; Rosa26R-stop-YFP mice in two established models of fibrosis: cardiac ischaemic injury and kidney ureteric occlusion. In both cardiac and kidney fibrosis, lineage tracing showed a significant subpopulation of endothelial-derived cells expressed mesenchymal markers, indicating they had undergone EndMT. In addition, miR-126-3p was restricted to endothelial cells and down-regulated in murine fibrotic kidney and heart tissue. These findings were confirmed in patient kidney biopsies. MiR-126-3p expression is restricted to endothelial cells and is down-regulated during EndMT. Over-expression of miR-126-3p reduces EndMT, therefore, it could be considered for miRNA-based therapeutics in fibrotic organs. [ABSTRACT FROM AUTHOR]
Copyright of International Journal of Molecular Sciences is the property of MDPI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: MiR-126-3p Is Dynamically Regulated in Endothelial-to-Mesenchymal Transition during Fibrosis.
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  Data: <searchLink fieldCode="AR" term="%22Jordan%2C+Nina+P%2E%22">Jordan, Nina P.</searchLink><br /><searchLink fieldCode="AR" term="%22Tingle%2C+Samuel+J%2E%22">Tingle, Samuel J.</searchLink><br /><searchLink fieldCode="AR" term="%22Shuttleworth%2C+Victoria+G%2E%22">Shuttleworth, Victoria G.</searchLink><br /><searchLink fieldCode="AR" term="%22Cooke%2C+Katie%22">Cooke, Katie</searchLink><br /><searchLink fieldCode="AR" term="%22Redgrave%2C+Rachael+E%2E%22">Redgrave, Rachael E.</searchLink><br /><searchLink fieldCode="AR" term="%22Singh%2C+Esha%22">Singh, Esha</searchLink><br /><searchLink fieldCode="AR" term="%22Glover%2C+Emily+K%2E%22">Glover, Emily K.</searchLink><br /><searchLink fieldCode="AR" term="%22Ahmad+Tajuddin%2C+Hafiza+B%2E%22">Ahmad Tajuddin, Hafiza B.</searchLink><br /><searchLink fieldCode="AR" term="%22Kirby%2C+John+A%2E%22">Kirby, John A.</searchLink><br /><searchLink fieldCode="AR" term="%22Arthur%2C+Helen+M%2E%22">Arthur, Helen M.</searchLink><br /><searchLink fieldCode="AR" term="%22Ward%2C+Chris%22">Ward, Chris</searchLink><br /><searchLink fieldCode="AR" term="%22Sheerin%2C+Neil+S%2E%22">Sheerin, Neil S.</searchLink><br /><searchLink fieldCode="AR" term="%22Ali%2C+Simi%22">Ali, Simi</searchLink>
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  Data: International Journal of Molecular Sciences; Aug2021, Vol. 22 Issue 16, p8629-8629, 1p
– Name: Subject
  Label: Subject Terms
  Group: Su
  Data: <searchLink fieldCode="DE" term="%22RENAL+fibrosis%22">RENAL fibrosis</searchLink><br /><searchLink fieldCode="DE" term="%22FIBROSIS%22">FIBROSIS</searchLink><br /><searchLink fieldCode="DE" term="%22RENAL+biopsy%22">RENAL biopsy</searchLink><br /><searchLink fieldCode="DE" term="%22HEART+fibrosis%22">HEART fibrosis</searchLink><br /><searchLink fieldCode="DE" term="%22HEART+injuries%22">HEART injuries</searchLink><br /><searchLink fieldCode="DE" term="%22ENDOTHELIAL+cells%22">ENDOTHELIAL cells</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: In fibrotic diseases, myofibroblasts derive from a range of cell types including endothelial-to-mesenchymal transition (EndMT). Increasing evidence suggests that miRNAs are key regulators in biological processes but their profile is relatively understudied in EndMT. In human umbilical vein endothelial cells (HUVEC), EndMT was induced by treatment with TGFβ2 and IL1β. A significant decrease in endothelial markers such as VE-cadherin, CD31 and an increase in mesenchymal markers such as fibronectin were observed. In parallel, miRNA profiling showed that miR-126-3p was down-regulated in HUVECs undergoing EndMT and over-expression of miR-126-3p prevented EndMT, maintaining CD31 and repressing fibronectin expression. EndMT was investigated using lineage tracing with transgenic Cdh5-Cre-ERT2; Rosa26R-stop-YFP mice in two established models of fibrosis: cardiac ischaemic injury and kidney ureteric occlusion. In both cardiac and kidney fibrosis, lineage tracing showed a significant subpopulation of endothelial-derived cells expressed mesenchymal markers, indicating they had undergone EndMT. In addition, miR-126-3p was restricted to endothelial cells and down-regulated in murine fibrotic kidney and heart tissue. These findings were confirmed in patient kidney biopsies. MiR-126-3p expression is restricted to endothelial cells and is down-regulated during EndMT. Over-expression of miR-126-3p reduces EndMT, therefore, it could be considered for miRNA-based therapeutics in fibrotic organs. [ABSTRACT FROM AUTHOR]
– Name: Abstract
  Label:
  Group: Ab
  Data: <i>Copyright of International Journal of Molecular Sciences is the property of MDPI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.3390/ijms22168629
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        Text: English
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        StartPage: 8629
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      – SubjectFull: RENAL fibrosis
        Type: general
      – SubjectFull: FIBROSIS
        Type: general
      – SubjectFull: RENAL biopsy
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      – SubjectFull: HEART fibrosis
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      – SubjectFull: ENDOTHELIAL cells
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              Text: Aug2021
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