Specific premature epigenetic aging of cartilage in osteoarthritis

Osteoarthritis (OA) is a disease affecting multiple tissues of the joints in the elderly, but most notably articular cartilage. Premature biological aging has been described in this tissue and in blood cells, suggesting a systemic component of premature aging in the pathogenesis of OA. Here, we have...

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Autores: Vidal Bralo, L, López Golán, Y, Mera Varela, A, Rego Pérez, Ignacio, Horvath, S, Zhang, Y, Real Bolt, Álvaro del|||0000-0002-1057-461X, Zhai, G, Blanco, FJ, Riancho Moral, José Antonio|||0000-0003-0691-8755, Gómez Reino, JJ, González, A
Tipo de recurso: artículo
Fecha de publicación:2016
País:España
Institución:Universidad de Cantabria (UC)
Repositorio:UCrea Repositorio Abierto de la Universidad de Cantabria
Idioma:inglés
OAI Identifier:oai:repositorio.unican.es:10902/9265
Acceso en línea:http://hdl.handle.net/10902/9265
Access Level:acceso abierto
Palabra clave:Osteoarthritis
Biological age
Epigenetics
DNA methylation
Telomere length shortening
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spelling Specific premature epigenetic aging of cartilage in osteoarthritisVidal Bralo, LLópez Golán, YMera Varela, ARego Pérez, IgnacioHorvath, SZhang, YReal Bolt, Álvaro del|||0000-0002-1057-461XZhai, GBlanco, FJRiancho Moral, José Antonio|||0000-0003-0691-8755Gómez Reino, JJGonzález, AOsteoarthritisBiological ageEpigeneticsDNA methylationTelomere length shorteningOsteoarthritis (OA) is a disease affecting multiple tissues of the joints in the elderly, but most notably articular cartilage. Premature biological aging has been described in this tissue and in blood cells, suggesting a systemic component of premature aging in the pathogenesis of OA. Here, we have explored epigenetic aging in OA at the local (cartilage and bone) and systemic (blood) levels. Two DNA methylation age‐measures (DmAM) were used: the multi‐tissue age estimator for cartilage and bone; and a blood‐specific biomarker for blood. Differences in DmAM between OA patients and controls showed an accelerated aging of 3.7 years in articular cartilage (95 % CI = 1.1 to 6.3, P = 0.008) of OA patients. By contrast, no difference in epigenetic aging was observed in bone (0.04 years; 95 % CI = ‐1.8 to 1.9, P = 0.3) and in blood (‐0.6 years; 95 % CI = ‐1.5 to 0.3, P = 0.2) between OA patients and controls. Therefore, premature epigenetic aging according to DNA methylation changes was specific of OA cartilage, adding further evidence and insight on premature aging of cartilage as a component of OA pathogenesis that reflects damage and vulnerability.Impact Journals, LLCUniversidad de Cantabria20162016-01-01journal articlehttp://purl.org/coar/resource_type/c_6501NAhttp://purl.org/coar/version/c_be7fb7dd8ff6fe43info:eu-repo/semantics/articlehttp://hdl.handle.net/10902/9265Aging (Albany NY). 2016 Sep 28;8(9):2222-2231reponame:UCrea Repositorio Abierto de la Universidad de Cantabriainstname:Universidad de Cantabria (UC)Inglésengopen accesshttp://purl.org/coar/access_right/c_abf2Atribución 3.0 Españahttp://creativecommons.org/licenses/by/3.0/es/info:eu-repo/semantics/openAccessoai:repositorio.unican.es:10902/92652026-06-02T12:39:31Z
dc.title.none.fl_str_mv Specific premature epigenetic aging of cartilage in osteoarthritis
title Specific premature epigenetic aging of cartilage in osteoarthritis
spellingShingle Specific premature epigenetic aging of cartilage in osteoarthritis
Vidal Bralo, L
Osteoarthritis
Biological age
Epigenetics
DNA methylation
Telomere length shortening
title_short Specific premature epigenetic aging of cartilage in osteoarthritis
title_full Specific premature epigenetic aging of cartilage in osteoarthritis
title_fullStr Specific premature epigenetic aging of cartilage in osteoarthritis
title_full_unstemmed Specific premature epigenetic aging of cartilage in osteoarthritis
title_sort Specific premature epigenetic aging of cartilage in osteoarthritis
dc.creator.none.fl_str_mv Vidal Bralo, L
López Golán, Y
Mera Varela, A
Rego Pérez, Ignacio
Horvath, S
Zhang, Y
Real Bolt, Álvaro del|||0000-0002-1057-461X
Zhai, G
Blanco, FJ
Riancho Moral, José Antonio|||0000-0003-0691-8755
Gómez Reino, JJ
González, A
author Vidal Bralo, L
author_facet Vidal Bralo, L
López Golán, Y
Mera Varela, A
Rego Pérez, Ignacio
Horvath, S
Zhang, Y
Real Bolt, Álvaro del|||0000-0002-1057-461X
Zhai, G
Blanco, FJ
Riancho Moral, José Antonio|||0000-0003-0691-8755
Gómez Reino, JJ
González, A
author_role author
author2 López Golán, Y
Mera Varela, A
Rego Pérez, Ignacio
Horvath, S
Zhang, Y
Real Bolt, Álvaro del|||0000-0002-1057-461X
Zhai, G
Blanco, FJ
Riancho Moral, José Antonio|||0000-0003-0691-8755
Gómez Reino, JJ
González, A
author2_role author
author
author
author
author
author
author
author
author
author
author
dc.contributor.none.fl_str_mv Universidad de Cantabria
dc.subject.none.fl_str_mv Osteoarthritis
Biological age
Epigenetics
DNA methylation
Telomere length shortening
topic Osteoarthritis
Biological age
Epigenetics
DNA methylation
Telomere length shortening
description Osteoarthritis (OA) is a disease affecting multiple tissues of the joints in the elderly, but most notably articular cartilage. Premature biological aging has been described in this tissue and in blood cells, suggesting a systemic component of premature aging in the pathogenesis of OA. Here, we have explored epigenetic aging in OA at the local (cartilage and bone) and systemic (blood) levels. Two DNA methylation age‐measures (DmAM) were used: the multi‐tissue age estimator for cartilage and bone; and a blood‐specific biomarker for blood. Differences in DmAM between OA patients and controls showed an accelerated aging of 3.7 years in articular cartilage (95 % CI = 1.1 to 6.3, P = 0.008) of OA patients. By contrast, no difference in epigenetic aging was observed in bone (0.04 years; 95 % CI = ‐1.8 to 1.9, P = 0.3) and in blood (‐0.6 years; 95 % CI = ‐1.5 to 0.3, P = 0.2) between OA patients and controls. Therefore, premature epigenetic aging according to DNA methylation changes was specific of OA cartilage, adding further evidence and insight on premature aging of cartilage as a component of OA pathogenesis that reflects damage and vulnerability.
publishDate 2016
dc.date.none.fl_str_mv 2016
2016-01-01
dc.type.none.fl_str_mv journal article
http://purl.org/coar/resource_type/c_6501
NA
http://purl.org/coar/version/c_be7fb7dd8ff6fe43
dc.type.openaire.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv http://hdl.handle.net/10902/9265
url http://hdl.handle.net/10902/9265
dc.language.none.fl_str_mv Inglés
eng
language_invalid_str_mv Inglés
language eng
dc.rights.none.fl_str_mv open access
http://purl.org/coar/access_right/c_abf2
Atribución 3.0 España
http://creativecommons.org/licenses/by/3.0/es/
dc.rights.openaire.fl_str_mv info:eu-repo/semantics/openAccess
rights_invalid_str_mv open access
http://purl.org/coar/access_right/c_abf2
Atribución 3.0 España
http://creativecommons.org/licenses/by/3.0/es/
eu_rights_str_mv openAccess
dc.publisher.none.fl_str_mv Impact Journals, LLC
publisher.none.fl_str_mv Impact Journals, LLC
dc.source.none.fl_str_mv Aging (Albany NY). 2016 Sep 28;8(9):2222-2231
reponame:UCrea Repositorio Abierto de la Universidad de Cantabria
instname:Universidad de Cantabria (UC)
instname_str Universidad de Cantabria (UC)
reponame_str UCrea Repositorio Abierto de la Universidad de Cantabria
collection UCrea Repositorio Abierto de la Universidad de Cantabria
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,301603

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