Recent publications
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Interviews of the CIG PIs: F.Preitner

Series of interviews were written to present each PI of the CIG.
Most of them are already available on the new CIG Report’s website, and every week we will be displaying one of them in the newsletter.

The Mouse Metabolic Facility (MEF)

Dr. Frédéric Preitner, Maître d’Enseignement et de Recherche, is Supervisor of the Mouse Metabolic Facility (MEF) from UNIL-CHUV, which provides customized services to researchers in both fundamental and medical research. To that end, a wide repertoire of in vivo techniques and blood assays to analyse the phenotype of mouse models for obesity and diabetes has been established, and new technologies are implemented as required for each individual project. In addition, the MEF staff provides scientific support during data generation and analysis, as well as in the form of teaching and consulting.
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Cell Rep.: co-auth.: I.Xenarios

 2018 Apr 10;23(2):622-636. doi: 10.1016/j.celrep.2018.03.029.

Deciphering the Dynamic Transcriptional and Post-transcriptional Networks of Macrophages in the Healthy Heart and after Myocardial Injury.

Author information

1
Myocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), 28029 Madrid, Spain.
2
Vital-IT, SIB Swiss Institute of Bioinformatics, University of Lausanne, 1015 Lausanne, Switzerland.
3
Vascular Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), 28029 Madrid, Spain.
4
Bioinformatics Unit, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), 28029 Madrid, Spain. Electronic address: fscabo@cnic.es.
5
Myocardial Pathophysiology Area, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), 28029 Madrid, Spain. Electronic address: mricote@cnic.es.

Abstract

Macrophage plasticity has been studied in vitro, but transcriptional regulation upon injury is poorly understood. We generated a valuable dataset that captures transcriptional changes in the healthy heart and after myocardial injury, revealing a dynamic transcriptional landscape of macrophage activation. Partial deconvolution suggested that post-injury macrophages exhibit overlapping activation of pro-inflammatory and anti-inflammatory programs rather than aligning to canonical M1/M2 programs. Furthermore, simulated dynamics and experimental validation of a regulatory core of the underlying gene-regulatory network revealed a negative-feedback loop that limits initial inflammation via hypoxia-mediated upregulation of Il10. Our results also highlight the prominence of post-transcriptional regulation (miRNAs, mRNA decay, and lincRNAs) in attenuating the myocardial injury-induced inflammatory response. We also identified a cardiac-macrophage-specific gene signature (e.g., Egfr and Lifr) and time-specific markers for macrophage populations (e.g., Lyve1, Cd40, and Mrc1). Altogether, these data provide a core resource for deciphering the transcriptional network in cardiac macrophages in vivo.

KEYWORDS:

Boolean dynamical model; IL-10; heart; lincRNAs; miRnome; myocardial injury; partial deconvolution; transcriptome analysis

PMID: 29642017

 

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D-Day 2018 : April 26, 2018. CHUV – Register now

Registration : http://wp.unil.ch/dday/registration/
Deadline: April 13, 201

D-Day 2018

Jacques Dubochet – Nobel Prize in Chemistry 2017, Dept. of Ecology and Evolution, UNIL, Switzerland

Silvia Monticelli – Institute for Research in Biomedicine, USI, Bellinzona, Switzerland
John P. Carr – Dept. of Plant Sciences, University of Cambridge, UK
Collin Ewald – Dept. of Health Sciences and Technology, ETH, Zürich, Switzerland

On Thursday April 26th, 2018 the 14th edition of the D.Day will take place!

This event is organized by the Association of PhD students and Assistants of the Faculty of Biology and Medicine and supported by the Doctoral school of the faculty.

D.Day is a research day whose aim is to illustrate the wide variety of the topics studied in the Faculty, either via poster presentations or lectures given by scientists of international renown.

Moreover, like last year, the committee will select some PhD students who would like to give an oral presentation about their research.

The participation with presentation of a poster is credited by 0.5 credits for the FBM PhD Doctoral School (cf. “general information”). In addition, PhD students exhibiting the best posters or the best oral presentations will receive an award!

Even though most of the participants are PhD students or post-docs, the D.Day is open to all scientists. Participants from other institutions than UNIL are also more than welcome to join us!

Supported by the Doctoral School of the FBM, the D.Day is a well recognized research event. We are looking forward to meeting you there!

The organizing committee

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L.Michalik will give a talk, 13:30 on April 27, 2018, Aud. E.Jequier-Doge, BH08 (CHUV)

DrSc. Liliane Michalik (Centre intégratif de génomique)

Leçon pour les étudiant·e·s : « La peau et ses réponses aux agressions de l’environnement »

 Séminaire de recherche : « PPARs control skin responses to UV and skin carcinogenesis »

Auditoire E. Jequier-Doge – BH08
Vendredi 27 avril 2018
13h30 – 15h00

***********

Cette leçon  est organisée dans le cadre de la Commission d’appel pour un poste de Professeure associée, responsable de la coordination, du développement stratégique et des enseignements institutionnels, basé au Centre intégratif de génomique

 


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Research Associate/Senior Research Associate in Genomics, Newcastle University (UK)

Location: Newcastle University, Newcastle upon Tyne, NE1 7RU
Research Associate/Senior Research Associate in Genomics – A118207R

See online vacancy at: https://vacancies.ncl.ac.uk/LoginV2.aspx

 

Closing date: 27 April 2018

Salary:
Research Associate (Grade F): £29,799 – £38,833
Senior Research Associate (Grade G): £39,992 – £47,722

You will join a multidisciplinary team within The Institute of Genetic Medicine lead by Professor J Veltman to work on the genomics of male infertility. You will carry out genomics and transcriptomics studies in material derived from infertile men and their family members and will work on improving and enhancing the integration of these omics approaches and interpretation of their results in the clinical context .You will design follow-up studies to establish the function of novel male infertility genes and the mechanisms underlying this condition. The overall aims of the research is to identify novel genetic causes of male infertility, improve the genetic diagnostics in infertile men, identify risk factors that increase the risk of male infertility in their offspring, and  find novel targets for treatment.

You will have a PhD in a relevant subject area, along with a Bachelor’s degree (or equivalent) in a science, medicine or health-related subject. At Senior Research Associate level, postdoctoral experience in relevant research fields e.g. genomics or transcriptomics is essential, as well as evidence of a record of research including publication and presentation of data at conferences.

You will have high level laboratory skills, in particular in genomics or transcriptomics, as well as the ability to communicate complex information clearly both orally and in writing. Strong critical thinking skills are essential, as well as evidence of good skills in writing scientific publications.

The grade of appointment will be based on experience and qualifications.

This post is tenable until 31st July 2020.

For further information about the post please contact Professor J Veltman – Institute Director on joris.veltman@ncl.ac.uk

 

 

Prof.dr. Joris A. Veltman

Director, Institute of Genetic Medicine, Newcastle University

Royal Society Wolfson Research Merit Award Holder

Jacobson chair of Personalized Medicine

 

Biomedicine West Wing

International Centre for Life

Central Parkway NE13BZ

Newcastle-upon-Tyne

United Kingdom

E-mail: joris.veltman@newcastle.ac.uk

 

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Cell Discov.: co-auth.: W.Wahli

 2018 Apr 3;4:15. doi: 10.1038/s41421-018-0014-5. eCollection 2018.

Selective deletion of PPARβ/δ in fibroblasts causes dermal fibrosis by attenuated LRG1 expression.

Sng MK1,2Chan JSK1Teo Z1Phua T1,3Tan EHP1Wee JWK1Koh NJN1Tan CK2Chen JP2Pal M4Tong BMK5Tnay YL5Ng XR2Zhu P1Chiba S5Wang X2,6,7,8Wahli W2,9,10Tan NS1,2,6,11.

Abstract

Connective tissue diseases of the skin are characterized by excessive collagen deposition in the skin and internal organs. Fibroblasts play a pivotal role in the clinical presentation of these conditions. Nuclear receptor peroxisome-proliferator activated receptors (PPARs) are therapeutic targets for dermal fibrosis, but the contribution of the different PPAR subtypes are poorly understood. Particularly, the role of fibroblast PPARβ/δ in dermal fibrosis has not been elucidated. Thus, we generated a mouse strain with selective deletion of PPARβ/δ in the fibroblast (FSPCre-Pparb/d-/-) and interrogated its epidermal and dermal transcriptome profiles. We uncovered a downregulated gene, leucine-rich alpha-2-glycoprotein-1 (Lrg1), of previously unknown function in skin development and architecture. Our findings suggest that the regulation of Lrg1 by PPARβ/δ in fibroblasts is an important signaling conduit integrating PPARβ/δ and TGFβ1-signaling networks in skin health and disease. Thus, the FSPCre-Pparb/d-/- mouse model could serve as a novel tool in the current gunnery of animal models to better understand dermal fibrosis.

PMID: 29619245