Laurent Metzinger

ORCID: 0000-0002-7636-8480
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About
Contact & Profiles
Research Areas
  • MicroRNA in disease regulation
  • Circular RNAs in diseases
  • Cancer-related molecular mechanisms research
  • Muscle Physiology and Disorders
  • Adipose Tissue and Metabolism
  • RNA modifications and cancer
  • RNA and protein synthesis mechanisms
  • Exercise and Physiological Responses
  • Extracellular vesicles in disease
  • Cardiac Valve Diseases and Treatments
  • RNA Research and Splicing
  • Cardiovascular Disease and Adiposity
  • Erythrocyte Function and Pathophysiology
  • Parathyroid Disorders and Treatments
  • interferon and immune responses
  • Bacterial Genetics and Biotechnology
  • Diabetes Treatment and Management
  • Aortic Thrombus and Embolism
  • Aortic aneurysm repair treatments
  • Erythropoietin and Anemia Treatment
  • Cardiovascular Function and Risk Factors
  • Bone and Joint Diseases
  • Sirtuins and Resveratrol in Medicine
  • Liver Disease Diagnosis and Treatment
  • Hemoglobinopathies and Related Disorders

Université de Picardie Jules Verne
2015-2024

Hématopoïèse et immunologie
2016-2023

Centre Hospitalier Universitaire Amiens-Picardie
2011-2021

Université Sorbonne Paris Nord
2011-2021

Sorbonne Université
2021

Inserm
2009-2019

Mécanismes physiopathologiques et conséquences des calcifications cardiovasculaires
2017

Sorbonne Paris Cité
2017

Physiopathologie et Epidémiologie des Maladies Respiratoires
2016-2017

Laboratoire de Biochimie
2012

Utrophin is a dystrophin-related cytoskeletal protein expressed in many tissues. It thought to link F-actin the internal cytoskeleton transmembrane complex similar dystrophin (DPC). At adult neuromuscular junction (NMJ), utrophin precisely colocalized with acetylcholine receptors (AChRs) and recent studies have suggested role for AChR cluster formation or maintenance during NMJ differentiation. We disrupted expression by gene targeting mouse. Such mice no detectable Western blotting...

10.1083/jcb.136.4.883 article EN The Journal of Cell Biology 1997-02-24

Backgound An elevated serum inorganic phosphate (Pi) level is a major risk factor for kidney disease and downstream vascular complications. We focused on the effect of Pi levels human aortic smooth muscle cells (VSMCs), with an emphasis role microRNAs (miRNAs). Methodology/Principal Findings Exposure primary VSMCs in vitro to pathological increased calcification, migration rate concomitantly reduced cell proliferation amount actin cytoskeleton. These changes were evidenced by significant...

10.1371/journal.pone.0047807 article EN cc-by PLoS ONE 2012-10-18

Abstract Several microRNAs (miRNAs) have been linked to chronic kidney disease (CKD) mortality, cardiovascular (CV) complications and progression. However, their association with clinical outcomes remains poorly evaluated. We used real-time qPCR measure serum levels of miR-126 miR-223 in a large cohort 601 CKD patients (CKD stage G1 G5 or on renal replacement therapy – G5D) from Ghent University Hospital 31 healthy controls. All-cause mortality events were registered as endpoints over 6 year...

10.1038/s41598-019-41101-8 article EN cc-by Scientific Reports 2019-03-14

Morphology and changes in gene expression of vascular endothelium are mainly due to shear stress inflammation. Cell phenotype modulation has been clearly demonstrated be controlled by small noncoding micro-RNAs (miRNAs). This study focused on the effect laminar (LSS) human endothelial cells (HUVECs), with an emphasis role miRNA-126 (miR-126). Exposure HUVECs vitro LSS modified shape concomitantly regulated miR-126, cell adhesion molecule 1 (VCAM-1), syndecan-4 (SDC-4). A significant...

10.1155/2015/497280 article EN cc-by BioMed Research International 2015-01-01

Vascular calcification (VC) is prevalent in patients suffering from chronic kidney disease (CKD). High phosphate levels promote VC by inducing abnormalities mineral and bone metabolism. Previously, we demonstrated that magnesium (Mg(2+)) prevents inorganic phosphate- (Pi-) induced human aortic vascular smooth muscle cells (HAVSMC). As microRNAs (miR) modulate gene expression, investigated the role of miR-29b, -30b, -125b, -133a, -143, -204 protective effect Mg(2+) on VC. HAVSMC were cultured...

10.1155/2016/7419524 article EN BioMed Research International 2016-01-01

In Duchenne muscular dystrophy (DMD) dysregulation of cytosolic calcium appears to be involved in the degeneration skeletal muscle fibres. Therefore, we have studied regulation free concentration ([Ca 2+ ] c ) under specific stress conditions cultured myotubes isolated from hind limbs wild‐type (C57BL10) and dystrophin‐deficient mutant mdx mice. [Ca was estimated by use Ca ‐sensitive fluorescent dye, fura‐2. Resting similar normal (35 ± 9 nM 38 nM, respectively). However, when were exposed a...

10.1111/j.1476-5381.1996.tb15445.x article EN British Journal of Pharmacology 1996-06-01

Mutations in the genes encoding dystrophin or dystrophin-associated proteins are responsible for Duchenne muscular dystrophy various forms of limb-girdle dystrophies respectively. We have recently cloned gene murine 87 kDa postsynaptic protein dystrobrevin, a protein. Anti-dystrobrevin antibodies stain sarcolemma normal skeletal muscle indicating that dystrobrevin co-localises with and complex. By contrast, membrane staining is severely reduced muscles patients, consistent being...

10.1093/hmg/6.7.1185 article EN Human Molecular Genetics 1997-07-01
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