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Inhibition of MicroRNA-125a Promotes Human Endothelial Cell Proliferation and Viability through an Antiapoptotic Mechanism.

Svensson, Daniel LU ; Gidlöf, Olof LU ; Turczynska, Karolina LU ; Erlinge, David LU ; Albinsson, Sebastian LU and Nilsson, Bengt-Olof LU (2014) In Journal of Vascular Research 51(3). p.239-245
Abstract
The microRNA-125a (miR-125a) is highly expressed in endothelial cells, but its role in vascular biology is not known. Endothelial cell proliferation and viability play an important role in endothelial healing, and we hypothesize that miR-125a regulates this process. The aim of the present study was to investigate if miR-125a controls human endothelial cell proliferation, viability and endothelial healing, and to assess the mechanisms involved. We showed that overexpression of miR-125a by transfection with miR-125a mimic reduced human umbilical vein endothelial cell (HUVEC) proliferation and viability, and stimulated apoptosis as demonstrated by a miR-125a-induced increase of the proportion of annexin V-positive cells monitored by flow... (More)
The microRNA-125a (miR-125a) is highly expressed in endothelial cells, but its role in vascular biology is not known. Endothelial cell proliferation and viability play an important role in endothelial healing, and we hypothesize that miR-125a regulates this process. The aim of the present study was to investigate if miR-125a controls human endothelial cell proliferation, viability and endothelial healing, and to assess the mechanisms involved. We showed that overexpression of miR-125a by transfection with miR-125a mimic reduced human umbilical vein endothelial cell (HUVEC) proliferation and viability, and stimulated apoptosis as demonstrated by a miR-125a-induced increase of the proportion of annexin V-positive cells monitored by flow cytometry. Moreover, we showed that the miR-125a mimic downregulated the antiapoptotic Bcl2 protein and upregulated caspase 3, suggesting that these two proteins represent molecular targets for miR-125a. Accordingly, transfection with miR-125a inhibitor, downregulating miR-125a expression, promoted HUVEC proliferation and viability, and reduced apoptosis. Importantly, transfection with miR-125a inhibitor promoted HUVEC tube formation in Matrigel, suggesting that reduction of miR-125a has a proangiogenic effect. In conclusion, downregulation of miR-125a through local transfection with miR-125a inhibitor might be a new way to enhance endothelial cell proliferation and viability, thereby promoting the reendothelialization observed in response to intimal injury. © 2014 S. Karger AG, Basel. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Vascular Research
volume
51
issue
3
pages
239 - 245
publisher
Karger
external identifiers
  • pmid:25116893
  • wos:000341169000008
  • scopus:84906039533
ISSN
1423-0135
DOI
10.1159/000365551
language
English
LU publication?
yes
id
995c4cf6-de44-4f81-b3f6-bbc086aabe56 (old id 4614834)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/25116893?dopt=Abstract
date added to LUP
2014-09-06 23:01:04
date last changed
2017-10-22 03:12:40
@article{995c4cf6-de44-4f81-b3f6-bbc086aabe56,
  abstract     = {The microRNA-125a (miR-125a) is highly expressed in endothelial cells, but its role in vascular biology is not known. Endothelial cell proliferation and viability play an important role in endothelial healing, and we hypothesize that miR-125a regulates this process. The aim of the present study was to investigate if miR-125a controls human endothelial cell proliferation, viability and endothelial healing, and to assess the mechanisms involved. We showed that overexpression of miR-125a by transfection with miR-125a mimic reduced human umbilical vein endothelial cell (HUVEC) proliferation and viability, and stimulated apoptosis as demonstrated by a miR-125a-induced increase of the proportion of annexin V-positive cells monitored by flow cytometry. Moreover, we showed that the miR-125a mimic downregulated the antiapoptotic Bcl2 protein and upregulated caspase 3, suggesting that these two proteins represent molecular targets for miR-125a. Accordingly, transfection with miR-125a inhibitor, downregulating miR-125a expression, promoted HUVEC proliferation and viability, and reduced apoptosis. Importantly, transfection with miR-125a inhibitor promoted HUVEC tube formation in Matrigel, suggesting that reduction of miR-125a has a proangiogenic effect. In conclusion, downregulation of miR-125a through local transfection with miR-125a inhibitor might be a new way to enhance endothelial cell proliferation and viability, thereby promoting the reendothelialization observed in response to intimal injury. © 2014 S. Karger AG, Basel.},
  author       = {Svensson, Daniel and Gidlöf, Olof and Turczynska, Karolina and Erlinge, David and Albinsson, Sebastian and Nilsson, Bengt-Olof},
  issn         = {1423-0135},
  language     = {eng},
  number       = {3},
  pages        = {239--245},
  publisher    = {Karger},
  series       = {Journal of Vascular Research},
  title        = {Inhibition of MicroRNA-125a Promotes Human Endothelial Cell Proliferation and Viability through an Antiapoptotic Mechanism.},
  url          = {http://dx.doi.org/10.1159/000365551},
  volume       = {51},
  year         = {2014},
}