📇 Rhumatologue · BRON CEDEX · (69) · Salarié

MME Lola LESSARD

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3 raisons identifiées

Plateau technique de référence
Hospices Civils de Lyon (HCL) — équipements et expertise pointus pour les cas complexes
Praticien-chercheur
12 articles scientifiques publiés — formation continue solide
Délais de RDV courts dans la région
144.6 rhumatos / 100 000 hab. — département bien doté

Rhumatologue

📍 BRON CEDEX (69)SalariéRPPS 10111663885

Publications actives

2ans d'exercice (thèse 2024)·21 publications sur 5 ans

📊 Reconnaissance scientifique : 6/100📝 24 articles publiés🇫🇷 Publications académiques françaises (7)

✨ Génération du profil synthétique IA en cours…

Données ANS publiques (Licence Ouverte 2.0) · Enrichissements MonRhumato 100 % opt-in · Toute personne référencée peut demander la suppression ou la rectification.

Top publications · les plus citées

The efficacy of cryotherapy following arthroscopic knee surgery

The Journal of orthopaedic and sports physical therapy · 1997

📚 41 citations🎯 RCR 2.65Top 19% NIH🩺 Clinique

CD109 overexpression ameliorates skin fibrosis in a mouse model of bleomycin-induced scleroderma

Arthritis and rheumatism · 2013

📚 25 citations

Lire l'abstract Crossref ↓

AbstractObjectiveTransforming growth factor β (TGFβ) is a profibrotic cytokine, and its aberrant function is implicated in several types of fibrotic pathologies including scleroderma (systemic sclerosis [SSc]). Multiple lines of evidence show that increased TGFβ signaling contributes to progressive fibrosis in SSc by promoting fibroblast activation, excessive extracellular matrix (ECM) deposition, and dermal thickening. We have previously identified CD109 as a TGFβ coreceptor and have shown that it antagonizes TGFβ signaling and TGFβ‐induced ECM expression in vitro in human keratinocytes and fibroblasts. The aim of the present study was to examine the ability of CD109 to prevent skin fibrosis in a mouse model of bleomycin‐induced SSc.MethodsTransgenic mice overexpressing CD109 in the epidermis and their wild‐type (WT) littermates were injected with bleomycin in phosphate buffered saline (PBS) or with PBS alone every other day for 21 days or 28 days. Dermal thickness and collagen deposition were determined histologically using Masson's trichrome and picrosirius red staining. In addition, collagen and fibronectin content was analyzed using Western blotting, and activation of TGFβ signaling was examined by determining phospho‐Smad2 and phospho‐Smad3 levels using Western blotting and immunohistochemistry.ResultsTransgenic mice overexpressing CD109 in the epidermis showed resistance to bleomycin‐induced skin fibrosis, as evidenced by a significant decrease in dermal thickness, collagen crosslinking, collagen and fibronectin content, and phospho‐Smad2/3 levels, as compared to their WT littermates.ConclusionOur findings suggest that CD109 inhibits TGFβ signaling and fibrotic responses in experimental murine scleroderma. They also suggest that CD109 regulates dermal–epidermal interactions to decrease extracellular matrix synthesis in the dermis. Thus, CD109 is a potential molecular target for therapeutic intervention in scleroderma.

Contribution of major histocompatibility complex class II immunostaining in distinguishing idiopathic inflammatory myopathy subgroups: A histopathological cohort study

Journal of neuropathology and experimental neurology · 2024

📚 9 citations🎯 RCR 2.37Top 22% NIH🔓 Open Access📄 PDF gratuit ↗

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Abstract Idiopathic inflammatory myopathies (IIM) are rare, acquired muscle diseases; their diagnosis of is based on clinical, serological, and histological criteria. MHC-I-positive immunostaining, although non-specific, is used as a marker for IIM diagnosis; however, the significance of major histocompatibility complex (MHC)-II immunostaining in IIM remains debated. We investigated patterns of MHC-II immunostaining in myofibers and capillaries in muscle biopsies from 103 patients with dermatomyositis ([DM], n = 31), inclusion body myositis ([IBM], n = 24), anti-synthetase syndrome ([ASyS], n = 10), immune-mediated necrotizing myopathy ([IMNM], n = 18), or overlap myositis ([OM], n = 20). MHC-II immunostaining of myofibers was abnormal in 63/103 of patients (61%) but the patterns differed according to the IIM subgroup. They were diffuse in IBM (96%), negative in IMNM (83%), perifascicular in ASyS (70%), negative (61%) or perifascicular (32%) in DM, and either clustered (40%), perifascicular (30%), or diffuse heterogeneous (15%) in OM. Capillary MHC-II immunostaining also identified quantitative (capillary dropout, n = 47/88, 53%) and qualitative abnormalities, that is, architectural abnormalities, including dilated and leaky capillaries, (n = 79/98, 81%) in all IIM subgroups. Thus, MHC-II myofiber expression patterns allow distinguishing among IIM subgroups. We suggest the addition of MHC-II immunostaining to routine histological panels for IIM diagnosis.

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MME Lola LESSARD

Pourquoi vous devez consulter ce praticien

Thèses universitaires

Activité de recherche & publications

Publications académiques en France

Lieu de consultation

Tarifs & secteur de conventionnement

Prendre rendez-vous & contact

Top publications · les plus citées

Publications scientifiques (12) — classées par pathologie

Transversal4

Case report / série3

Épidémiologie & registres2

Activité physique / Rééducation1

Revue générale1

Sclérodermie1

Vascularites des gros vaisseaux1

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