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Mohammad Al Tarrass
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| PhD in Cell Biology | |
| LinkedIn: Mohammad-al-tarrass ; ORCID: 0009-0003-9337-9100 |
Biography
Mohammad Al Tarrass is a passionate early-stage researcher with a strong background in biochemistry, cell biology, and expertise in vascular biology. He holds a Bachelor's degree in Biochemistry from Lebanese University and completed a double diploma Master’s degree in Healthy Living Technologies with honors in 2019, through a collaborative program between Lebanese University (Lebanon) and the University of Grenoble Alpes (France). During this program, he performed his Master's internship at the Biomics Lab (CEA Grenoble), where he investigated the DNA-dependent protease SPRTN as a therapeutic target in cancer.
Following this, Mohammad began his PhD at CEA Grenoble-Biosanté, working within the BMP family in the angiogenesis and lymphangiogenesis team (BAL). His research focused on deciphering phosphoproteomic changes in response to BMP9 and BMP10 in endothelial cells. The aim was to understand the role of these ligands in vascular homeostasis and propose novel therapeutic approaches for treating rare vascular diseases, particularly Hereditary Hemorrhagic Telangiectasia (HHT) and Pulmonary Arterial Hypertension (PAH), which are associated with defects in their signaling pathways. He successfully obtained his PhD in Cell Biology from the University of Grenoble Alpes in 2023.
Throughout his scientific career, Mohammad has gained significant experience in various aspects of cellular biology, utilizing a wide range of molecular and biochemical techniques alongside advanced technologies (Mass-spectrometry). He has published three scientific papers, a book chapter, and presented his research at several national and international conferences (Researchgate).
In addition to his role in the MIMOSA project, Dr Al Tarrass is developing and validating, together with Dr Thomas Duflot, an analytical method for analyzing sphingosine and sphingosine-1-phosphate (S1P) species in biological samples (in vivo or in vitro models of cardiovascular disease) using liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS). He will also investigate the role of S1P signaling in vascular endothelial cells and its significance in maintaining vascular and lymphatic barriers. This work builds on ongoing international projects led by the EnVI laboratory, including ANR PHASM (Dr Jeremy Bellien) and ANR CITE-LYMPH (Dr Ebba Brakenhielm).
Inserm U1096 in the news
Previous media articles on our research:
- Memory services for Pr Alain Cribier Décès du Professeur Alain Cribier - Université de Rouen Normandie (univ-rouen.fr), Hommage au Professeur Alain Cribier (chu-rouen.fr)
- Highlight on chronic kidney disease by lab member Pr D Guerrot
- Highlight of our preclinical research in The Conversation
- Projet FHU CARNAVAL
- FASEB BIOART 2020
- RHU STOP-AS (@RHU_STOPAS) | FDNitter
- Projet RHU STOP-AS sélectioné
- Un reseau invisible au secours du coeur
- Prix Jean-Paul Binet
- Ma thèse en 180 secondes
- Prix "Don de soi -don de vie"
- Réseau ERA-CVD LYMIT-DIS
- Réseau FHU REMOD-VHF
- Helene Eltchaninoff, membre de la Fédération Hospitalo-Universitaire - Portail vidéo de l'Université de Rouen Normandie (univ-rouen.fr)
Epigenetic check-point regulates polarization of monocytes post-MI
Myocardial infarction (MI) triggers a wound healing response that involves rapid recruitment of immune cells, notably myeloid cells, to the heart. This innate immune response is required for efficient healing, and alteration of its kinetics may contribute to poor infarct remodeling driving heart failure development. In the latest issue of Nature Communications, the team led by Dr. Fraineau described for the first time the role of an epigenetic switch in regulating the kinetics and profiles of the innate immune response post-MI. Specifically, they uncovered that an epigenetic transcriptional repressive enzyme, named EZH2, serves as an epigenetic check-point during polarization of monocytes toward an immunomodulatory pro-regenerative macrophage phenotype. Using an epigenetic pharmacological inhibitor of EZH2, this check-point can be suppressed, thus enhancing the transcriptomic program resulting in generation of more immunomodulatory macrophages. This led to an acceleration of the innate immune response after MI, resulting in reduced deleterious infarct scar remodeling, and prevention of post-MI aggravation of cardiac dysfunction. Altogether, Fraineau et al. identified an original epigenetic mechanism governing macrophage polarization toward either proinflammatory or immunomodulatory phenotypes, thus revealing epigenetic mechanisms as a novel therapeutic target to improve inflammatory kinetics post-MI to prevent heart failure development.
See further: open access article or video presentation by Dr Fraineau
