Extracellular Uridine Triphosphate and Adenosine Triphosphate Attenuate Endothelial Inflammation through miR-22-Mediated ICAM-1 Inhibition.
(2015) In Journal of Vascular Research 52(2). p.71-80- Abstract
- Adenosine and uridine triphosphate (ATP and UTP) can act as extracellular signalling molecules, playing important roles in vascular biology and disease. ATP and UTP acting via the P2Y2-receptor have, for example, been shown to regulate endothelial dilatation, inflammation and angiogenesis. MicroRNAs (miRNAs), a class of regulatory, short, non-coding RNAs, have been shown to be important regulators of these biological processes. In this study, we used RNA deep-sequencing to explore changes in miRNA expression in the human microvascular endothelial cell line HMEC-1 upon UTP treatment. The expression of miR-22, which we have previously shown to target ICAM-1 mRNA in HMEC-1, increased significantly after stimulation. Up-regulation of miR-22... (More)
- Adenosine and uridine triphosphate (ATP and UTP) can act as extracellular signalling molecules, playing important roles in vascular biology and disease. ATP and UTP acting via the P2Y2-receptor have, for example, been shown to regulate endothelial dilatation, inflammation and angiogenesis. MicroRNAs (miRNAs), a class of regulatory, short, non-coding RNAs, have been shown to be important regulators of these biological processes. In this study, we used RNA deep-sequencing to explore changes in miRNA expression in the human microvascular endothelial cell line HMEC-1 upon UTP treatment. The expression of miR-22, which we have previously shown to target ICAM-1 mRNA in HMEC-1, increased significantly after stimulation. Up-regulation of miR-22 and down-regulation of cell surface ICAM-1 were confirmed with qRT-PCR and flow cytometry, respectively. siRNA-mediated knockdown of the P2Y2-receptor abolished the effect of UTP on miR-22 transcription. Leukocyte adhesion was significantly inhibited in HMEC-1 following miR-22 overexpression and treatment with UTP/ATP. In conclusion, extracellular UTP and ATP can attenuate ICAM-1 expression and leukocyte adhesion in endothelial cells through miR-22. © 2015 S. Karger AG, Basel. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/7476252
- author
- Gidlöf, Olof LU ; Sathanoori, Ramasri LU ; Magistri, Marco ; Faghihi, Mohammad Ali ; Wahlestedt, Claes ; Olde, Björn LU and Erlinge, David LU
- organization
- publishing date
- 2015
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Journal of Vascular Research
- volume
- 52
- issue
- 2
- pages
- 71 - 80
- publisher
- Karger
- external identifiers
-
- pmid:26088024
- wos:000362541900001
- scopus:84931843852
- pmid:26088024
- ISSN
- 1423-0135
- DOI
- 10.1159/000431367
- language
- English
- LU publication?
- yes
- id
- 542de6a6-e1aa-4ee2-9372-b404dfb58034 (old id 7476252)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/26088024?dopt=Abstract
- date added to LUP
- 2016-04-01 09:57:46
- date last changed
- 2022-02-24 21:03:37
@article{542de6a6-e1aa-4ee2-9372-b404dfb58034, abstract = {{Adenosine and uridine triphosphate (ATP and UTP) can act as extracellular signalling molecules, playing important roles in vascular biology and disease. ATP and UTP acting via the P2Y2-receptor have, for example, been shown to regulate endothelial dilatation, inflammation and angiogenesis. MicroRNAs (miRNAs), a class of regulatory, short, non-coding RNAs, have been shown to be important regulators of these biological processes. In this study, we used RNA deep-sequencing to explore changes in miRNA expression in the human microvascular endothelial cell line HMEC-1 upon UTP treatment. The expression of miR-22, which we have previously shown to target ICAM-1 mRNA in HMEC-1, increased significantly after stimulation. Up-regulation of miR-22 and down-regulation of cell surface ICAM-1 were confirmed with qRT-PCR and flow cytometry, respectively. siRNA-mediated knockdown of the P2Y2-receptor abolished the effect of UTP on miR-22 transcription. Leukocyte adhesion was significantly inhibited in HMEC-1 following miR-22 overexpression and treatment with UTP/ATP. In conclusion, extracellular UTP and ATP can attenuate ICAM-1 expression and leukocyte adhesion in endothelial cells through miR-22. © 2015 S. Karger AG, Basel.}}, author = {{Gidlöf, Olof and Sathanoori, Ramasri and Magistri, Marco and Faghihi, Mohammad Ali and Wahlestedt, Claes and Olde, Björn and Erlinge, David}}, issn = {{1423-0135}}, language = {{eng}}, number = {{2}}, pages = {{71--80}}, publisher = {{Karger}}, series = {{Journal of Vascular Research}}, title = {{Extracellular Uridine Triphosphate and Adenosine Triphosphate Attenuate Endothelial Inflammation through miR-22-Mediated ICAM-1 Inhibition.}}, url = {{http://dx.doi.org/10.1159/000431367}}, doi = {{10.1159/000431367}}, volume = {{52}}, year = {{2015}}, }