MicroRNA markers of inflammation and remodelling in temporal arteries from patients with giant cell arteritis

Croci, Stefania; Zerbini, Alessandro; Boiardi, Luigi; Muratore, Francesco; Bisagni, Alessandra; Nicoli, Davide; Farnetti, Enrico; Pazzola, Giulia; Cimino, Luca; Moramarco, Antonio; Cavazza, Alberto; Casali, Bruno; Parmeggiani, Maria; Salvarani, Carlo

doi:10.1136/annrheumdis-2015-207846

Cited by 41 publications

(41 citation statements)

References 48 publications

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“…Recently 6 miRNAs have been found overexpressed in inflamed TAs from GCA patients compared to non-inflamed, normal TAs: miR146b-5p, -146a, -21, -150, -155, -299-5p [102]. Noteworthy, miR146b-5p, -146a, -21 and -155 have been found overexpressed also in abdominal aortic aneurysms and atherosclerotic plaques indicating an overlap between pathogenetic mechanisms in GCA and other inflammatory cardiovascular diseases.…”

Section: Mirna Overexpression In Gcamentioning

confidence: 99%

“…Expression of miR-146b-5p, 146a, -21 and -155 is at a downstream point of the activation of Nuclear Factor-κB (NF-κB), TLRs and signal transducer and activator of transcription 3 (STAT3) suggesting that these pathways might be involved in GCA pathogenesis. Noteworthy such miRNAs can be induced by cellular senescence and inflammation [102]. Moreover, arterial wall cells such as VSMCs, endothelial cells and adventitial fibroblasts can also express them.…”

Section: Mirna Overexpression In Gcamentioning

confidence: 99%

“…It is actually unknown whether such miRNAs are biomarkers of specific infiltrating immune cell subsets and activated pathways in inflamed TAs and/or have a functional role in GCA pathogenesis. MiR-146a, -21, -155 and -150 can be expressed by specific immune cell subsets [102]. MiR-155 is mainly a pro-inflammatory miRNA, miR-21 can have both pro-and anti-inflammatory activities whereas miR-146a and miR-150 mainly restrain inflammation by negative feedback circuits.…”

Section: Mirna Overexpression In Gcamentioning

confidence: 99%

See 2 more Smart Citations

New insights into the pathogenesis of giant cell arteritis

Ciccia

Rizzo

Ferrante

et al. 2017

Autoimmunity Reviews

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Section: Mirna Overexpression In Gcamentioning

confidence: 99%

Section: Mirna Overexpression In Gcamentioning

confidence: 99%

Section: Mirna Overexpression In Gcamentioning

confidence: 99%

See 1 more Smart Citation

New insights into the pathogenesis of giant cell arteritis

Ciccia

Rizzo

Ferrante

et al. 2017

Autoimmunity Reviews

Self Cite

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“…Thus, methylation regulation of NFAT may be crucial in driving the activation of Th17 cells in GCA. Only one report of dysregulated miRNA has been published in GCA and this study found that miRNA-21 was dysregulated in GCA temporal biopsies [94]. miRNA-21 was overexpressed in the biopsies and this appears to be tissue specific, as the use of PBMCs derived from the same donors when compared across groups demonstrated no difference.…”

Section: Giant Cell Arteritismentioning

confidence: 65%

“…miRNA-21 was overexpressed in the biopsies and this appears to be tissue specific, as the use of PBMCs derived from the same donors when compared across groups demonstrated no difference. These data suggest that the increase of miRNA-21 level is tissue specific [94]. To this day only, a handful of studies have looked at the epigenome in GCA and this is a rich area for research.…”

Section: Giant Cell Arteritismentioning

confidence: 99%

Epigenetic Modulation as a Therapeutic Prospect for Treatment of Autoimmune Rheumatic Diseases

Ciechomska

O’Reilly

2016

Mediators of Inflammation

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Systemic inflammatory rheumatic diseases are considered as autoimmune diseases, meaning that the balance between recognition of pathogens and avoidance of self-attack is impaired and the immune system attacks and destroys its own healthy tissue. Treatment with conventional Disease Modifying Antirheumatic Drugs (DMARDs) and/or Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) is often associated with various adverse reactions due to unspecific and toxic properties of those drugs. Although biologic drugs have largely improved the outcome in many patients, such drugs still pose significant problems and fail to provide a solution to all patients. Therefore, development of more effective treatments and improvements in early diagnosis of rheumatic diseases are badly needed in order to increase patient's functioning and quality of life. The reversible nature of epigenetic mechanisms offers a new class of drugs that modulate the immune system and inflammation. In fact, epigenetic drugs are already in use in some types of cancer or cardiovascular diseases. Therefore, epigenetic-based therapeutics that control autoimmunity and chronic inflammatory process have broad implications for the pathogenesis, diagnosis, and management of rheumatic diseases. This review summarises the latest information about potential therapeutic application of epigenetic modification in targeting immune abnormalities and inflammation of rheumatic diseases.

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Altered Plasma Levels and Tissue Expression of Fibroblast Activation Protein Alpha in Giant Cell Arteritis

Xu,

Jiemy,

Boots

et al. 2024

Arthritis Care & Research

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ObjectiveGiant cell arteritis (GCA) is characterized by granulomatous inflammation of the medium and large‐sized arteries accompanied by remodeling of the vessel wall. Fibroblast activation protein alpha (FAP) is a serine protease which promotes both inflammation and fibrosis. Here we investigated the plasma levels and vascular expression of FAP in GCA.MethodsPlasma FAP levels were measured with ELISA in treatment‐naive GCA (n=60) and polymyalgia rheumatica (PMR, n=63) patients (compared to age‐ and sex‐matched healthy controls (HC), n=42) and during follow‐up, including treatment free remission (TFR). Inflamed temporal artery biopsies (TAB) of GCA patients (n=9), non‐inflamed TAB (n=14), aorta samples from GCA‐ (n=9) and atherosclerosis‐related aneurysm (n=11) were stained for FAP using immunohistochemistry. Immunofluorescence staining was performed for fibroblasts(CD90), macrophages(CD68/CD206/FRβ), vascular smooth muscle cells(desmin), myofibroblasts(αSMA), interleukin(IL)‐6 and matrix metalloproteinase(MMP)‐9.ResultsBaseline plasma FAP levels were significantly lower in GCA compared to PMR patients and HC, and inversely correlated with systemic markers of inflammation and angiogenesis. FAP levels decreased even further at 3 months upon remission in GCA, and gradually increased to the level of HC in TFR. FAP expression was increased in inflamed TAB and aorta of GCA patients compared with control tissues. FAP was abundantly expressed in fibroblasts and macrophages. Part of the FAP+ fibroblasts expressed IL‐6 and MMP‐9.ConclusionFAP expression in GCA is clearly modulated both in plasma and in vessels. FAP may be involved in the inflammatory and remodeling processes in GCA and have utility as target for imaging and therapeutic intervention.image

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MicroRNA markers of inflammation and remodelling in temporal arteries from patients with giant cell arteritis

Abstract: MiR-146b-5p, -146a, -21, -150, -155, -299-5p are overexpressed in the presence of inflammation in TABs from patients with GCA.

Cited by 41 publications

References 48 publications

New insights into the pathogenesis of giant cell arteritis

New insights into the pathogenesis of giant cell arteritis

Epigenetic Modulation as a Therapeutic Prospect for Treatment of Autoimmune Rheumatic Diseases

Altered Plasma Levels and Tissue Expression of Fibroblast Activation Protein Alpha in Giant Cell Arteritis

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