📇 Rhumatologue · PARIS · (75) · Libéral
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2 raisons identifiées
Praticien-chercheur
12 articles scientifiques publiés — formation continue solide
Délais de RDV courts dans la région
336.2 rhumatos / 100 000 hab. — département bien doté
✨ Génération du profil synthétique IA en cours…
CABINET DU DR MICHEL BROCK
151 RUE DU FAUBOURG SAINT ANTOINE, 75011 PARIS
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Arthritis and rheumatism · 2010
AbstractObjectiveTo investigate the role of microRNA (miRNA) as posttranscriptional regulators of profibrotic genes in systemic sclerosis (SSc).MethodsMicroRNA, which target collagens, were identified by in silico analysis. Expression of miRNA‐29 (miR‐29) was determined by TaqMan real‐time polymerase chain reaction analysis of skin biopsy and fibroblast samples from SSc patients and healthy controls as well as in the mouse model of bleomycin‐induced skin fibrosis. Cells were transfected with precursor miRNA (pre‐miRNA)/anti‐miRNA of miR‐29 using Lipofectamine. Collagen gene expression was also studied in luciferase reporter gene assays. For stimulation, recombinant transforming growth factor β (TGFβ), platelet‐derived growth factor B (PDGF‐B), or interleukin‐4 (IL‐4) was used. The effects of inhibiting PDGF‐B and TGFβ signaling on the levels of miR‐29 were studied in vitro and in the bleomycin model.ResultsWe found that miR‐29a was strongly down‐regulated in SSc fibroblasts and skin sections as compared with the healthy controls. Overexpression in SSc fibroblasts significantly decreased, and accordingly, knockdown in normal fibroblasts increased, the levels of messenger RNA and protein for type I and type III collagen. In the reporter gene assay, cotransfection with pre‐miR‐29a significantly decreased the relative luciferase activity, which suggests a direct regulation of collagen by miR‐29a. TGFβ, PDGF‐B, or IL‐4 reduced the levels of miR‐29a in normal fibroblasts to those seen in SSc fibroblasts. Similar to human SSc, the expression of miR‐29a was reduced in the bleomycin model of skin fibrosis. Inhibition of PDGF‐B and TGFβ pathways by treatment with imatinib restored the levels of miR‐29a in vitro and in the bleomycin model in vivo.ConclusionThese data add the posttranscriptional regulation of collagens by miR‐29a as a novel aspect to the fibrogenesis of SSc and suggest miR‐29a as a potential therapeutic target.
Arthritis and rheumatism · 2007
Abstract Objective Rheumatoid arthritis (RA) is a chronic inflammatory disorder of unknown origin. Histone deacetylase (HDA) activity is considered to play a major role in the transcriptional regulation of proinflammatory genes. We undertook this study to investigate the balance of histone acetylase and HDA activity in synovial tissue from RA patients compared with that from patients with osteoarthritis (OA) and normal controls. Methods Activity of histone acetylases and HDAs was measured in nuclear extracts of total synovial tissue samples, which were obtained from RA and OA patients undergoing surgical joint replacement, and compared with the activity in synovial tissues from patients without arthritis. Tissue expression of HDAs 1 and 2 was quantified by Western blotting. In addition, immunohistochemistry was performed for HDA‐2. Results Mean ± SEM HDA activity in synovial tissue samples derived from patients with RA was measured as 1.5 ± 0.3 μmoles/μg, whereas the activity levels in OA (3.2 ± 0.7 μmoles/μg) and normal (7.1 ± 4.2 μmoles/μg) synovial tissue samples were significantly higher. Histone acetylase activity reached similar levels in RA and OA tissues and in normal tissues. The ratio of HDA activity to histone acetylase activity in RA synovial tissue was significantly reduced (12 ± 2%) compared with that in OA synovial tissue (26 ± 3%). The activity ratio in normal control samples was arbitrarily set at 100 ± 40%. In addition, the tissue expression of HDA‐1 and HDA‐2 proteins was clearly lower in RA samples than in OA samples. Conclusion The balance of histone acetylase/HDA activities is strongly shifted toward histone hyperacetylation in patients with RA. These results offer novel molecular insights into the pathogenesis of the disease that might be relevant to the development of future therapeutic approaches.
Arthritis and rheumatism · 2013
AbstractObjectiveTo elucidate whether the microRNA (miRNA) cluster miR‐17–92 contributes to the activated phenotype of rheumatoid arthritis synovial fibroblasts (RASFs).MethodsRASFs were stimulated with tumor necrosis factor α (TNFα), and the expression and regulation of the miR‐17–92 cluster were studied using real‐time quantitative PCR (PCR) and promoter activity assays. RASFs were transfected with single precursor molecules of miRNAs from miR‐17–92 and the expression of matrix‐degrading enzymes and cytokines was measured by quantitative PCR and enzyme‐linked immunosorbent assay. Potential miRNA targets were identified by computational prediction and were validated using reporter gene assays and Western blotting. The activity of NF‐κB signaling was determined by reporter gene assays.ResultsWe found that TNFα induces the expression of miR‐17–92 in RASFs in an NF‐κB–dependent manner. Transfection of RASFs with precursor molecules of single members of miR‐17–92 revealed significantly increased expression levels of matrix‐degrading enzymes, proinflammatory cytokines, and chemokines in precursor miR‐18a (pre‐miR‐18a)–transfected RASFs. Using reporter gene assays, we identified the NF‐κB pathway inhibitor TNFα‐induced protein 3 as a new target of miR‐18a. In addition, pre‐miR‐18a–transfected RASFs showed stronger activation of NF‐κB signaling, both constitutively and in response to TNFα stimulation.ConclusionOur data suggest that the miR‐17–92–derived miR‐18a contributes to cartilage destruction and chronic inflammation in the joint through a positive feedback loop in NF‐κB signaling, with concomitant up‐regulation of matrix‐degrading enzymes and mediators of inflammation in RASFs.
Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).
bioRxiv : the preprint server for biology · 2026 · Journal Article
Michel J, Forjaz A, Queiroga V, Casella K, et al.
Nature human behaviour · 2024 · Historical Article
Mushtaq F, Welke D, Gallagher A, Pavlov YG, et al.
Clinical EEG and neuroscience · 2013 · Journal Article
He BJ, Nolte G, Nagata K, Takano D, et al.
Arthritis and rheumatism · 2013 · Journal Article
Trenkmann M, Brock M, Gay RE, Michel BA, et al.
Annals of the rheumatic diseases · 2011 · Journal Article
Trenkmann M, Brock M, Gay RE, Kolling C, et al.
Arthritis research & therapy · 2011 · Conference Proceedings
Brock M, Trenkmann M, Filkova M, Hemmatazad H, et al.
Clinical reviews in allergy & immunology · 2010 · Journal Article
Trenkmann M, Brock M, Ospelt C, Gay S
Arthritis and rheumatism · 2010 · Journal Article
Maurer B, Stanczyk J, Jüngel A, Akhmetshina A, et al.
Arthritis and rheumatism · 2007 · Journal Article
Huber LC, Brock M, Hemmatazad H, Giger OT, et al.
Annals of the rheumatic diseases · 1977 · Comparative Study
Lovell CR, Brock M, Jayson MI, Baddeley H
Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 1997 · Journal Article
Thyss A, Suciu S, Bertrand Y, Mazingue F, et al.
Journal of pediatric gastroenterology and nutrition · 2025 · Journal Article
Davidson N, Morris GA, Wright MA, Brock G, et al.