Laure Rolland

ORCID: 0000-0003-3028-5329
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About
Contact & Profiles
Research Areas
  • Pancreatic function and diabetes
  • Metabolism, Diabetes, and Cancer
  • Diabetes Treatment and Management
  • Histone Deacetylase Inhibitors Research
  • Genetics and Neurodevelopmental Disorders
  • Diabetes and associated disorders
  • Liver Disease Diagnosis and Treatment
  • Epigenetics and DNA Methylation
  • Diet, Metabolism, and Disease
  • Mass Spectrometry Techniques and Applications
  • Cancer-related gene regulation
  • Error Correcting Code Techniques
  • RNA modifications and cancer
  • Neuroscience and Neural Engineering
  • Graphene and Nanomaterials Applications
  • Electrochemical sensors and biosensors
  • Immune cells in cancer
  • GABA and Rice Research
  • Multiple Sclerosis Research Studies
  • Diabetes Management and Research
  • Alzheimer's disease research and treatments
  • Endoplasmic Reticulum Stress and Disease
  • Peripheral Neuropathies and Disorders
  • Peptidase Inhibition and Analysis

Roche (France)
2025

Institut Pasteur de Lille
2015-2023

Centre Hospitalier Universitaire de Lille
2015-2023

Université de Lille
2014-2023

Inserm
2020-2023

Facteurs de risque et déterminants moléculaires des maladies liées au vieillissement
2022-2023

European Genomic Institute for Diabetes
2014-2022

Centre National de la Recherche Scientifique
2014-2022

(Epi)génomique fonctionnelle métabolique et des dysfonctions dans le diabète de type 2 et des maladies associées
2020-2022

In type 2 diabetes (T2D), hepatic insulin resistance is strongly associated with nonalcoholic fatty liver disease (NAFLD). this study, we hypothesized that the DNA methylome of livers from patients T2D compared individuals normal plasma glucose levels can unveil some mechanism could link to NAFLD. Using and transcriptome analyses obese individuals, found hypomethylation at a CpG site in PDGFA (encoding platelet-derived growth factor α) overexpression are both increased risk,...

10.2337/db17-1539 article EN Diabetes 2018-05-04

Type 2 diabetes is characterized by chronic hyperglycemia associated with impaired insulin action and secretion. Although the heritability of type high, environment, including blood components, could play a major role in development disease. Amongst environmental effects, epitranscriptomic modifications have been recently shown to affect gene expression glucose homeostasis. The epitranscriptome reversible chemical changes RNA, one most prevalent being m6A methylation RNA. Since pancreatic β...

10.3390/cells11020291 article EN cc-by Cells 2022-01-15

Elevation of the dietary saturated fatty acid palmitate contributes to reduction functional beta cell mass in pathogenesis type 2 diabetes. The diabetogenic effect is achieved by increasing death through induction endoplasmic reticulum (ER) stress markers including activating transcription factor 3 (Atf3) and CAAT/enhancer-binding protein homologous protein-10 (Chop). In this study, we investigated whether treatment cells with MS-275, a HDAC1 HDAC3 activity inhibitor which prevents elicited...

10.1155/2014/195739 article EN cc-by Journal of Diabetes Research 2014-01-01

An electrochemical insulin-delivery system based on reduced graphene oxide impregnated with insulin is described.

10.1039/c5cc05539c article EN Chemical Communications 2015-01-01

The glucagon-like peptide 1 (Glp-1) has emerged as a hormone with broad pharmacological potential in type 2 diabetes (T2D) treatment, notably by improving β cell functions. cell-cycle regulator and transcription factor E2f1 is involved glucose homeostasis modulating mass function. Here, we report that cell-specific genetic ablation of (E2f1β−/−) impairs associated decreased expression the Glp-1 receptor (Glp1r) E2f1β−/− pancreatic islets. Pharmacological inhibition E2F1 transcriptional...

10.1016/j.celrep.2022.111170 article EN cc-by-nc-nd Cell Reports 2022-08-01

Type 2 diabetes (T2D) is a metabolic disorder characterized by loss of pancreatic β-cell function, decreased insulin secretion and increased resistance, that affects more than 537 million people worldwide. Although several treatments are proposed to patients suffering from T2D, long-term control glycemia remains challenge. Therefore, identifying new potential drugs targets positively affect function crucial. Here, we developed an automated approach allow the identification compounds or genes...

10.3390/cells12060849 article EN cc-by Cells 2023-03-09

The loss of pancreatic β-cell identity has emerged as an important feature type 2 diabetes development, but the molecular mechanisms are still elusive. Here, we explore cell-autonomous role cell-cycle regulator and transcription factor E2F1 in maintenance identity, insulin secretion, glucose homeostasis. We show that β-cell–specific E2f1 function mice triggers intolerance associated with defective altered endocrine cell mass, downregulation many genes, concomitant increase non–β-cell...

10.2337/db22-0604 article EN Diabetes 2023-05-22

Alzheimer's disease (AD) is the leading cause of dementia. While impaired glucose homeostasis has been shown to increase AD risk and pathological loss tau function, latter suggested contribute emergence alterations observed in patients. However, links between impairments homeostasis, remain unclear. In this context, present study aimed at investigating metabolic phenotype a new knock-in (KI) mouse model, expressing, physiological level, human protein bearing P301L mutation under control...

10.3389/fnmol.2022.841892 article EN cc-by Frontiers in Molecular Neuroscience 2022-02-16

Histone deacetylases enzymes (HDACs) are chromatin modifiers that regulate gene expression through deacetylation of lysine residues within specific histone and non-histone proteins. A cell-specific pattern defines the identity insulin-producing pancreatic β cells, yet molecular networks driving this transcriptional specificity not fully understood. Here, we investigated HDAC-dependent mechanisms controlling β-cell function using pan-HDAC inhibitor trichostatin immunoprecipitation assays RNA...

10.1016/j.isci.2023.107231 article EN cc-by-nc-nd iScience 2023-06-30

Histone deacetylases (HDAC) enzymes are chromatin modifiers which directly regulate gene expression through deacetylation of lysine residues within specific histone and non-histone proteins. A cell-specific pattern defines the identity insulin-producing pancreatic β cells, yet molecular networks driving this transcriptional specificity not fully understood. Here, we investigated HDAC-dependent mechanisms controlling β-cell function using trichostatin (TSA), a pan-HDAC inhibitor. We observed...

10.2139/ssrn.4347242 preprint EN 2023-01-01

Abstract The loss of pancreatic β-cell identity emerges as an important feature type 2 diabetes development, but the molecular mechanisms are still elusive. Here, we explore cell-autonomous role cell cycle regulator and transcription factor E2F1 in maintenance insulin secretion. We show that β-cell-specific E2f1 function mice triggers glucose intolerance associated with defective secretion, altered α-to-β-cell ratio, a downregulation many genes concomitant increase non-β-cell markers....

10.1101/2020.10.14.339929 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2020-10-14

Abstract Type 2 diabetes (T2D) is a metabolic disorder characterized by loss of pancreatic β- cell function, decreased insulin secretion and increased resistance, that affects more than 400 million people worldwide. Although several treatments are proposed to patients suffering from T2D, long-term control glycemia remains challenge. Therefore, identifying new potential drugs targets positively affect β-cell function crucial. Here, we developed an automated approach allow the identification...

10.1101/2023.02.14.528514 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2023-02-15

<p>The loss of pancreatic β-cell identity emerges as an important feature type 2 diabetes development, but the molecular mechanisms are still elusive. Here, we explore cell-autonomous role cell cycle regulator and transcription factor E2F1 in maintenance identity, insulin secretion glucose homeostasis. We show that β-cell-specific <em>E2f1 </em>function mice triggers intolerance associated with defective secretion, altered endocrine mass, a downregulation many genes...

10.2337/figshare.22906517 preprint EN cc-by-nc-sa 2023-05-22

<p>The loss of pancreatic β-cell identity emerges as an important feature type 2 diabetes development, but the molecular mechanisms are still elusive. Here, we explore cell-autonomous role cell cycle regulator and transcription factor E2F1 in maintenance identity, insulin secretion glucose homeostasis. We show that β-cell-specific <em>E2f1 </em>function mice triggers intolerance associated with defective secretion, altered endocrine mass, a downregulation many genes...

10.2337/figshare.22906517.v1 preprint EN cc-by-nc-sa 2023-05-22

Type 2 diabetes (T2D) is closely linked with non-alcoholic fatty liver disease (NAFLD) and hepatic insulin resistance, but the involved mechanisms are still elusive. Using DNA methylome transcriptome analyses of livers from obese individuals, we found that both hypomethylation at a CpG site in PDGFA (encoding platelet derived growth factor alpha) overexpression associated increased T2D risk, hyperinsulinemia, resistance steatohepatitis risk. Both genetic risk score studies human cell...

10.48550/arxiv.1712.04680 preprint EN other-oa arXiv (Cornell University) 2017-01-01

Abstract Objective The pancreatic islets of Langerhans contain distinct cell subtypes including insulin-producing β cells. Although their cell-specific gene expression pattern defines identity, the underlying molecular network driving this transcriptional specificity is not fully understood. Among numerous regulators, histone deacetylases (HDAC) enzymes are potent chromatin modifiers which directly regulate through deacetylation lysine residues within specific proteins. precise mechanisms...

10.1101/2022.12.14.519294 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2022-12-15

Abstract Compromised β-cell function contributes to type 2 diabetes (T2D) development. The glucagon like peptide 1 (Glp-1) has emerged as a hormone with broad pharmacological potential toward T2D treatment, notably by improving functions. Recent data have shown that the transcription factor E2f1, besides its role cell cycle regulator, is involved in glucose homeostasis modulating mass, and identity. Here, we demonstrate crosstalk between E2F1, phosphorylation of retinoblastoma protein (pRb)...

10.1101/2021.04.16.440172 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2021-04-16

Compromised ß-cell function contributes to type 2 diabetes (T2D) development. The glucagon like peptide 1 (Glp-1) has emerged as a hormone with broad pharmacological potential toward T2D treatment, notably by improving functions. Recent data have shown that the transcription factor E2f1, besides its role cell cycle regulator, is involved in glucose homeostasis modulating mass, and identity. Here, we demonstrate crosstalk between E2F1, phosphorylation of retinoblastoma protein (pRb) Glp-1...

10.2139/ssrn.3855072 article EN SSRN Electronic Journal 2021-01-01
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