M PHILIPPE GUILLOT

Rhumatologue

RPPS 10002075488

📊 Reconnaissance scientifique : 12/100📝 106 articles publiés🇫🇷 Publications académiques françaises (8)

✨ Génération du profil synthétique IA en cours…

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Indicateurs publics agrégés sur 250 M+ d'œuvres scientifiques (OpenAlex, PubMed). Traduits ici en langage patient.

Influence scientifique

12 articles ont été cités au moins 12fois par d'autres chercheurs — preuve que ses travaux sont repris par la communauté médicale.

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Top publications · les plus citées

Primary Osteoporosis in Young Adults: Genetic Basis and Identification of Novel Variants in Causal Genes

JBMR plus · 2018

📚 47 citations🎯 RCR 1.94🔓 Open Access📄 PDF gratuit ↗

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ABSTRACTGenetic determinants contribute to osteoporosis and enhance the risk of fracture. Genomewide association studies of unselected population‐based individuals or families have identified polymorphisms in several genes related to low bone density, but not in osteoporotic patients with Z‐score < −2.0 SD with fragility fracture(s). The aim of this study was to determine the causal genes of idiopathic osteoporosis in the adulthood. Also, we used next‐generation sequencing of candidate genes in a cohort of 123 young or middle‐aged adults with idiopathic osteoporosis. All patients were included if they had a low bone mineral density (Z‐score < −2 SD), a diagnosis before age 55 years (mean ± SD, 48.4 ± 10.6 years; mean ± SD age at first fracture, 30.4 ± 17.4 years) and fracture or not. We found that 11 patients carried rare or novel variants in COL1A2 (n = 4), PLS3 (n = 2), WNT1 (n = 4), or DKK1 (n = 1). We showed a high prevalence of pathogenic variants in LRP5: 22 patients (17.8%) had the p.Val667Met variant, including three at the homozygous level and 16 (13%) carrying a novel or very rare variant. Functional analysis revealed that the LRP5 missense variants resulted in reduced luciferase activity, which indicates reduced activation of canonical WNT signaling. The clinical phenotype of patients carrying causal gene variants was indistinguishable. In conclusion, molecular screening of young osteoporotic adults revealed several variants and could be useful to characterize susceptibility genes for personalizing treatment, in particular for the new anabolic drugs.© 2017 The Authors. JBMR Plus is published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research.

Human fetal and adult bone marrow-derived mesenchymal stem cells use different signaling pathways for the initiation of chondrogenesis

Stem cells and development · 2014

📚 44 citations🎯 RCR 1.81🔓 Open Access

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Cartilage injuries and osteoarthritis are leading causes of disability in developed countries. The regeneration of damaged articular cartilage using cell transplantation or tissue engineering holds much promise but requires the identification of an appropriate cell source with a high proliferative propensity and consistent chondrogenic capacity. Human fetal mesenchymal stem cells (MSCs) have been isolated from a range of perinatal tissues, including first-trimester bone marrow, and have demonstrated enhanced expansion and differentiation potential. However, their ability to form mature chondrocytes for use in cartilage tissue engineering has not been clearly established. Here, we compare the chondrogenic potential of human MSCs isolated from fetal and adult bone marrow and show distinct differences in their responsiveness to specific growth factors. Transforming growth factor beta 3 (TGFβ3) induced chondrogenesis in adult but not fetal MSCs. In contrast, bone morphogenetic protein 2 (BMP2) induced chondrogenesis in fetal but not adult MSCs. When fetal MSCs co-stimulated with BMP2 and TGFβ3 were used for cartilage tissue engineering, they generated tissue with type II collagen and proteoglycan content comparable to adult MSCs treated with TGFβ3 alone. Investigation of the TGFβ/BMP signaling pathway showed that TGFβ3 induced phosphorylation of SMAD3 in adult but not fetal MSCs. These findings demonstrate that the initiation of chondrogenesis is modulated by distinct signaling mechanisms in fetal and adult MSCs. This study establishes the feasibility of using fetal MSCs in cartilage repair applications and proposes their potential as an in vitro system for modeling chondrogenic differentiation and skeletal development studies.

New pathogenic hypotheses for spondyloarthropathies

Joint bone spine · 2002

📚 19 citations

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M PHILIPPE GUILLOT

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Activité de recherche & publications

Publications académiques en France

Lieu de consultation

Tarifs & secteur de conventionnement

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Articles de presse (1)

Top publications · les plus citées

Publications scientifiques (23) — classées par pathologie

Transversal12

Gériatrie2

Ostéoporose2

Activité physique / Rééducation1

Anti-TNF1

Arthrite juvénile1

Essai clinique1

Génétique1

Goutte1

Spondyloarthrite1

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