Platelet transcriptional profile and protein expression in patients with systemic lupus erythematosus: up-regulation of the type I interferon system is strongly associated with vascular disease.
(2010) In Blood Jul 1. p.1951-1957- Abstract
- Patients with systemic lupus erythematosus (SLE) have a markedly increased risk to develop cardiovascular disease, and traditional cardiovascular risk factors fail to account for this increased risk. We used microarray to probe the platelet transcriptome in individuals with SLE and healthy controls, and the gene and protein expression of a subset of differentially expressed genes was further investigated and correlated to platelet activation status. Real-time PCR was used to confirm a type I interferon (IFN) gene signature in patients with SLE, and the IFN-regulated proteins PRKRA, IFITM1 and CD69 (p<0.0001) were found to be up-regulated in platelets from SLE patients as compared to healthy volunteers. Notably, patients with a history... (More)
- Patients with systemic lupus erythematosus (SLE) have a markedly increased risk to develop cardiovascular disease, and traditional cardiovascular risk factors fail to account for this increased risk. We used microarray to probe the platelet transcriptome in individuals with SLE and healthy controls, and the gene and protein expression of a subset of differentially expressed genes was further investigated and correlated to platelet activation status. Real-time PCR was used to confirm a type I interferon (IFN) gene signature in patients with SLE, and the IFN-regulated proteins PRKRA, IFITM1 and CD69 (p<0.0001) were found to be up-regulated in platelets from SLE patients as compared to healthy volunteers. Notably, patients with a history of vascular disease had increased expression of type I IFN-regulated proteins as well as more activated platelets as compared with patients without vascular disease. We suggest that interferogenic immune complexes stimulate production of IFNalpha which up-regulates the megakaryocytic type I IFN-regulated genes and proteins. This could affect platelet activation and contribute to development of vascular disease in SLE. In addition, platelets with type I IFN signature could be a novel marker for vascular disease in SLE. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1626187
- author
- Lood, Christian LU ; Amisten, Stefan LU ; Gullstrand, Birgitta LU ; Jönsen, Andreas LU ; Allhorn, Maria LU ; Truedsson, Lennart LU ; Sturfelt, Gunnar LU ; Erlinge, David LU and Bengtsson, Anders LU
- organization
- publishing date
- 2010
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Blood
- volume
- Jul 1
- pages
- 1951 - 1957
- publisher
- American Society of Hematology
- external identifiers
-
- wos:000282152000021
- pmid:20538795
- scopus:77956905671
- pmid:20538795
- ISSN
- 1528-0020
- DOI
- 10.1182/blood-2010-03-274605
- language
- English
- LU publication?
- yes
- id
- 4460dd46-8d33-4b17-8116-3ad4a1c6200b (old id 1626187)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/20538795?dopt=Abstract
- date added to LUP
- 2016-04-04 07:38:28
- date last changed
- 2022-04-23 08:23:53
@article{4460dd46-8d33-4b17-8116-3ad4a1c6200b, abstract = {{Patients with systemic lupus erythematosus (SLE) have a markedly increased risk to develop cardiovascular disease, and traditional cardiovascular risk factors fail to account for this increased risk. We used microarray to probe the platelet transcriptome in individuals with SLE and healthy controls, and the gene and protein expression of a subset of differentially expressed genes was further investigated and correlated to platelet activation status. Real-time PCR was used to confirm a type I interferon (IFN) gene signature in patients with SLE, and the IFN-regulated proteins PRKRA, IFITM1 and CD69 (p<0.0001) were found to be up-regulated in platelets from SLE patients as compared to healthy volunteers. Notably, patients with a history of vascular disease had increased expression of type I IFN-regulated proteins as well as more activated platelets as compared with patients without vascular disease. We suggest that interferogenic immune complexes stimulate production of IFNalpha which up-regulates the megakaryocytic type I IFN-regulated genes and proteins. This could affect platelet activation and contribute to development of vascular disease in SLE. In addition, platelets with type I IFN signature could be a novel marker for vascular disease in SLE.}}, author = {{Lood, Christian and Amisten, Stefan and Gullstrand, Birgitta and Jönsen, Andreas and Allhorn, Maria and Truedsson, Lennart and Sturfelt, Gunnar and Erlinge, David and Bengtsson, Anders}}, issn = {{1528-0020}}, language = {{eng}}, pages = {{1951--1957}}, publisher = {{American Society of Hematology}}, series = {{Blood}}, title = {{Platelet transcriptional profile and protein expression in patients with systemic lupus erythematosus: up-regulation of the type I interferon system is strongly associated with vascular disease.}}, url = {{http://dx.doi.org/10.1182/blood-2010-03-274605}}, doi = {{10.1182/blood-2010-03-274605}}, volume = {{Jul 1}}, year = {{2010}}, }