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Linked Open Data
'Atherothrombosis-associated microRNAs in Antiphospholipid syndrome and Systemic Lupus Erythematosus patients'.
Identificadores del recurso
http://hdl.handle.net/10668/10346
27502756
10.1038/srep31375
2045-2322
PMC4977549
https://www.nature.com/articles/srep31375.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4977549/pdf
Procedencia
(RISalud-ANDALUCÍA)

Ficha

Título:
'Atherothrombosis-associated microRNAs in Antiphospholipid syndrome and Systemic Lupus Erythematosus patients'.
Tema:
Adult
Antiphospholipid Syndrome
Autoantibodies
Biomarkers
Carotid Intima-Media Thickness
Case-Control Studies
Computational Biology
Epigenesis, Genetic
Female
Humans
Immunoglobulin G
Inflammation
Leukocytes
Lupus Erythematosus, Systemic
Male
MicroRNAs
Middle Aged
Monocytes
Neutrophils
Oxidative Stress
Thrombosis
Transfection
Descrición:
MicroRNAs markedly affect the immune system, and have a relevant role in CVD and autoimmune diseases. Yet, no study has analyzed their involvement in atherothrombosis related to APS and SLE patients. This study intended to: 1) identify and characterize microRNAs linked to CVD in APS and SLE; 2) assess the effects of specific autoantibodies. Six microRNAs, involved in atherothrombosis development, were quantified in purified leukocytes from 23 APS and 64 SLE patients, and 56 healthy donors. Levels of microRNAs in neutrophils were lower in APS and SLE than in healthy donors. Gene and protein expression of miRNA biogenesis-related molecules were also reduced. Accordingly, more than 75% of identified miRNAs by miRNA profiling were underexpressed. In monocytes, miR124a and -125a were low, while miR-146a and miR-155 appeared elevated. Altered microRNAs' expression was linked to autoimmunity, thrombosis, early atherosclerosis, and oxidative stress in both pathologies. In vitro treatment of neutrophils, monocytes, and ECs with aPL-IgG or anti-dsDNA-IgG antibodies deregulated microRNAs expression, and decreased miRNA biogenesis-related proteins. Monocyte transfections with pre-miR-124a and/or -125a caused reduction in atherothrombosis-related target molecules. In conclusion, microRNA biogenesis, significantly altered in neutrophils of APS and SLE patients, is associated to their atherothrombotic status, further modulated by specific autoantibodies.
Idioma:
Autor/Productor:
Pérez-Sánchez, C
Aguirre, M A
Ruiz-Limón, P
Barbarroja, N
Jiménez-Gómez, Y
de la Rosa, I Arias
Rodriguez-Ariza, A
Collantes-Estévez, E
Segui, P
Velasco, F
Cuadrado, M J
Teruel, R
González-Conejero, R
Martínez, C
López-Pedrera, Ch
Dereitos:
Attribution 4.0 International
http://creativecommons.org/licenses/by/4.0/
open access
Data:
2023-01-25T08:35:16Z
2016-08-09
Tipo de recurso:
research article
VoR
Formato:
application/pdf

oai_dc

Descargar XML

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    1. <dc:title>'Atherothrombosis-associated microRNAs in Antiphospholipid syndrome and Systemic Lupus Erythematosus patients'.</dc:title>

    2. <dc:creator>Pérez-Sánchez, C</dc:creator>

    3. <dc:creator>Aguirre, M A</dc:creator>

    4. <dc:creator>Ruiz-Limón, P</dc:creator>

    5. <dc:creator>Barbarroja, N</dc:creator>

    6. <dc:creator>Jiménez-Gómez, Y</dc:creator>

    7. <dc:creator>de la Rosa, I Arias</dc:creator>

    8. <dc:creator>Rodriguez-Ariza, A</dc:creator>

    9. <dc:creator>Collantes-Estévez, E</dc:creator>

    10. <dc:creator>Segui, P</dc:creator>

    11. <dc:creator>Velasco, F</dc:creator>

    12. <dc:creator>Cuadrado, M J</dc:creator>

    13. <dc:creator>Teruel, R</dc:creator>

    14. <dc:creator>González-Conejero, R</dc:creator>

    15. <dc:creator>Martínez, C</dc:creator>

    16. <dc:creator>López-Pedrera, Ch</dc:creator>

    17. <dc:subject>Adult</dc:subject>

    18. <dc:subject>Antiphospholipid Syndrome</dc:subject>

    19. <dc:subject>Autoantibodies</dc:subject>

    20. <dc:subject>Biomarkers</dc:subject>

    21. <dc:subject>Carotid Intima-Media Thickness</dc:subject>

    22. <dc:subject>Case-Control Studies</dc:subject>

    23. <dc:subject>Computational Biology</dc:subject>

    24. <dc:subject>Epigenesis, Genetic</dc:subject>

    25. <dc:subject>Female</dc:subject>

    26. <dc:subject>Humans</dc:subject>

    27. <dc:subject>Immunoglobulin G</dc:subject>

    28. <dc:subject>Inflammation</dc:subject>

    29. <dc:subject>Leukocytes</dc:subject>

    30. <dc:subject>Lupus Erythematosus, Systemic</dc:subject>

    31. <dc:subject>Male</dc:subject>

    32. <dc:subject>MicroRNAs</dc:subject>

    33. <dc:subject>Middle Aged</dc:subject>

    34. <dc:subject>Monocytes</dc:subject>

    35. <dc:subject>Neutrophils</dc:subject>

    36. <dc:subject>Oxidative Stress</dc:subject>

    37. <dc:subject>Thrombosis</dc:subject>

    38. <dc:subject>Transfection</dc:subject>

    39. <dc:description>MicroRNAs markedly affect the immune system, and have a relevant role in CVD and autoimmune diseases. Yet, no study has analyzed their involvement in atherothrombosis related to APS and SLE patients. This study intended to: 1) identify and characterize microRNAs linked to CVD in APS and SLE; 2) assess the effects of specific autoantibodies. Six microRNAs, involved in atherothrombosis development, were quantified in purified leukocytes from 23 APS and 64 SLE patients, and 56 healthy donors. Levels of microRNAs in neutrophils were lower in APS and SLE than in healthy donors. Gene and protein expression of miRNA biogenesis-related molecules were also reduced. Accordingly, more than 75% of identified miRNAs by miRNA profiling were underexpressed. In monocytes, miR124a and -125a were low, while miR-146a and miR-155 appeared elevated. Altered microRNAs' expression was linked to autoimmunity, thrombosis, early atherosclerosis, and oxidative stress in both pathologies. In vitro treatment of neutrophils, monocytes, and ECs with aPL-IgG or anti-dsDNA-IgG antibodies deregulated microRNAs expression, and decreased miRNA biogenesis-related proteins. Monocyte transfections with pre-miR-124a and/or -125a caused reduction in atherothrombosis-related target molecules. In conclusion, microRNA biogenesis, significantly altered in neutrophils of APS and SLE patients, is associated to their atherothrombotic status, further modulated by specific autoantibodies.</dc:description>

    40. <dc:date>2023-01-25T08:35:16Z</dc:date>

    41. <dc:date>2023-01-25T08:35:16Z</dc:date>

    42. <dc:date>2016-08-09</dc:date>

    43. <dc:type>research article</dc:type>

    44. <dc:type>VoR</dc:type>

    45. <dc:identifier>http://hdl.handle.net/10668/10346</dc:identifier>

    46. <dc:identifier>27502756</dc:identifier>

    47. <dc:identifier>10.1038/srep31375</dc:identifier>

    48. <dc:identifier>2045-2322</dc:identifier>

    49. <dc:identifier>PMC4977549</dc:identifier>

    50. <dc:identifier>https://www.nature.com/articles/srep31375.pdf</dc:identifier>

    51. <dc:identifier>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4977549/pdf</dc:identifier>

    52. <dc:language>en</dc:language>

    53. <dc:rights>Attribution 4.0 International</dc:rights>

    54. <dc:rights>http://creativecommons.org/licenses/by/4.0/</dc:rights>

    55. <dc:rights>open access</dc:rights>

    56. <dc:format>application/pdf</dc:format>

    </oai_dc:dc>

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