Differing patterns of peripheral blood leukocyte telomere length in rheumatologic diseases

Tamayo, María; Mosquera, Alejandro; Rego, José Ignacio; Fernández-Sueiro, José Luís; Blanco, Francisco J.; Fernández, José Luis Fernández

doi:10.1016/j.mrfmmm.2009.10.010

Cited by 34 publications

(38 citation statements)

References 35 publications

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“…On the contrary, other study proposes that the role of telomerase in the OA pathogenesis is still uncertain [32]. A recent work reported that telomere length of PBLs seemed not to be influenced by local OA pathology, confirming our present results; nevertheless, other rheumatologic diseases with higher and systemic inflammatory component, such as rheumatoid arthritis (RA), psoriatic arthritis (PA) and ankylosing spondilytis (AS) affected telomere length of PBLs, so that these patients showed longer telomere length than healthy controls [30]. However, the telomere length in OA chondrocytes is significantly shorter than in healthy aged chondrocytes, which may imply a local advance senescence that could contribute to the pathogenesis or progression of the OA disease [33].…”

Section: Discussionsupporting

confidence: 87%

“…On the contrary, this variability was not detected when analyzed the telomere length of PBL, and a consistent statistical association between the mtDNA haplogroup J and the telomere length was detected, clearly indicating that cells carrying this haplogroup suffer less oxidative stress. However, no differences in the telomere length of PBLs were detected between OA patients and healthy controls, as described earlier [30]. …”

Section: Discussionsupporting

confidence: 64%

“…The average telomere length of PBL was measured with a validated quantitative (Q-PCR)-based assay using a LightCycler 480 thermalcycler (Roche Diagnostics ® , Laval, Quebec, Canada) in a 96-well format, as described in Tamayo et al [30]. This method measures the average ratio of telomere repeat copy number to a single gene (36B4) copy number (T/S ratio) in each sample.…”

Section: Methodsmentioning

confidence: 99%

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mtDNA haplogroup J Modulates telomere length and Nitric Oxide production

Fernández-Moreno

Tamayo

Soto‐Hermida

et al. 2011

BMC Musculoskelet Disord

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BackgroundOxidative stress due to the overproduction of nitric oxide (NO) and other oxygen reactive species (ROS), play a main role in the initiation and progression of the OA disease and leads to the degeneration of mitochondria. Therefore, the goal of this work is to describe the difference in telomere length of peripheral blood leukocytes (PBLs) and Nitric Oxide (NO) production between mitochondrial DNA (mtDNA) haplogroup J and non-J carriers, as indirect approaches of oxidative stress.MethodsThe telomere length of PBL was analyzed in DNA samples from 166 healthy controls (114 J and 52 non-J) and 79 OA patients (41 J and 38 non-J) by means of a validated qPCR method. The NO production was assessed in 7 carriers of the haplogroup J and 27 non-J carriers, by means of the colorimetric reaction of the Griess reagent in supernatants of cultured chondrocytes. Inducible nitric oxide synthase (iNOS) mRNA from these samples was analyzed by qPCR. Appropiated statistical analyses were performedResultsCarriers of the haplogroup J showed a significantly longer telomere length of PBLs than non-J carriers, regardless of age, gender and diagnosis (p = 0.025). Cultured chondrocytes carrying the mtDNA haplogroup J also showed a lower NO production than non-J carriers (p = 0.043). No significant correlations between age and telomore length of PBLs were detected neither for carriers of the haplogroup J nor for non-J carriers. A strong positive correlation between NO production and iNOS expression was also observed (correlation coefficient = 0.791, p < 0.001).ConclusionThe protective effect of the mtDNA haplogroup J in the OA disease arise from a lower oxidative stress in carriers of this haplogroup, since this haplogroup is related to lower NO production and hence longer telomere length of PBLs too.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionsupporting

confidence: 64%

Section: Methodsmentioning

confidence: 99%

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mtDNA haplogroup J Modulates telomere length and Nitric Oxide production

Fernández-Moreno

Tamayo

Soto‐Hermida

et al. 2011

BMC Musculoskelet Disord

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“…Other clinical trials have demonstrated higher survival rates among individuals with high dietary intake of marine omega‐3 fatty acids and established cardiovascular diseases 33‐36 . Another study has found that leukocyte telomere shortening is associated with subtypes of rheumatologic diseases 37 …”

Section: Discussionmentioning

confidence: 99%

Shorter Telomere Length in Peripheral Blood Cells Associated With Migraine in Women

et al. 2010

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“…Carbamylation, like citrullination, is a post-translational modification in which lysine residues are converted to homocitrulline residues. Just as with ACPA, anti-CarP antibodies appear in the blood of RA patients several years before disease onset and, despite similarities shared with ACPA, they represent two independent systems, as suggested by the findings of patients presenting exclusively anti-CarP antibodies and not ACPA (45 (51,52). Clarification of similarities and differences in the pathogenic mechanisms underlying different types of RA-ILD may allow the identification of surrogate disease biomarkers to help clinicians in the early classification and stratification of patients with RA-ILD.…”

Section: Reviewmentioning

confidence: 99%

The onset site of rheumatoid arthritis: the joints or the lung?

et al. 2016

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The etiopathogenesis of rheumatoid arthritis (RA) is not yet fully elucidated and the site of inflammation onset is still a matter of debate. The presence of autoantibodies as well as clinical manifestations, such as interstitial lung disease, before the onset of arthritis seems to be in favour of the hypothesis that initial pathogenic events take place in tissues other than the joint. In this review article we summarize the most recent literature on extra-synovial autoimmunity triggers eventually leading to RA, with particular focus on the role of the lung. To date, anti-cyclic citrullinated peptide antibodies (ACPAs) are considered central players in RA pathogenesis and represent the gold-standard for disease diagnosis. Lungs and mucosae are exposed to environmental stimuli such as dusts and smoke which have been shown to foster citrullination of peptides in lungs thereby triggering the production of ACPA. In addition, other mechanisms of disease pathogenesis independent of citrullination play an important role. Deeper knowledge of these processes could represent a huge step forward in the management of RA, with dramatic impact on diagnosis, prevention, prognostic stratification and treatment of the disease.

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Differing patterns of peripheral blood leukocyte telomere length in rheumatologic diseases

Cited by 34 publications

References 35 publications

mtDNA haplogroup J Modulates telomere length and Nitric Oxide production

mtDNA haplogroup J Modulates telomere length and Nitric Oxide production

Shorter Telomere Length in Peripheral Blood Cells Associated With Migraine in Women

The onset site of rheumatoid arthritis: the joints or the lung?

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