CV Science

Pham My-Chan DANG Ph.D Phagocytes and NADPH oxidases in Inflammation.

Course and current status

2018-present: Research Director (DR2, CNRS) at Inserm U1149-CNRS ERL8252 /Research Center on Inflammation, Paris France. “Phagocytes and NADPH oxidases in Inflammation.” The team belongs to the Labex Inflamex (Laboratory of Excellence on Inflammation) contorsium.

2014- 2018: Research scientist (CR1, CNRS) at Inserm U1149-CNRS ERL8252 /Research Center on Inflammation, Paris France. “Regulation and role of NADPH Oxidases (NOXs) in inflammatory diseases”.

2007- 2014 : Research scientist (CR1, CNRS) at Inserm U773 / Bichat- Beaujon Biomedical Research Center, Paris France. “Activation mechanisms of NOX2 and NOX1 in phagocytes and epithelial cells”.

2002- 2007: Research scientist (CR1, CNRS) at Inserm U479, Paris France “Structure and activation of the phagocyte NADPH oxidase”.

2000- 2002 :   Postdoctoral position at Inserm U479, Paris France. “Regulation of the phagocyte NADPH oxidase by pro- and anti-inflammatory cytokines”. (Pr. Marie-Anne Gougerot-Pocidalo) Fellowship from la Fondation pour la Recherche Médicale.

1997- 2000 : Postdoctoral position at The Scripps Research Institute, La Jolla, California, USA.  Departement of Molecular and Experimental Medicine (Pr. Bernard Babior). “Assembly of the phagocyte NADPH oxidase.” Fellowship from the American Arthritis Foundation.

1993-1996 :   Ph.D in Life Sciences, University Paris XI, Orsay, France, “Protein kinase C and neutrophils activation”. Fellowship from the French Ministry of Higher Education.

Scientific activities and responsabilities.

- Direction and supervision of postdoctoral researchers, Ph. D students, invited scientists, master students, research engineers.

- Peer Review and editorial experiences :                                                               

• Reviewer for: Blood,  Scientific Reports, Journal of Immunology, Journal of Innate Immunity, FASEB Journal, Biochemical Pharmacology,  Medicinal Research Reviews, Journal of Leukocyte Biology….
• Editor in the scientific journal «Mediators of Inflammation ».
• Member of several Thesis Defence Committees. 

- Teaching: 

• Lecturer at the Master 2 « Neurosciences and Signaling », at the University of Paris-Saclay (Paris XI-Orsay).
• Lecturer at the Master 2 « Inflammation and Inflammatory diseases », organized by Labex Inflamex (Laboratory of Excellence on Inflammation), University of Paris (Paris Diderot).

- Committees and organization of meetings:

• Board member of the organizing committee of « the neutrophils club » affiliated to the French Society of Immunology (SFI) (2014-2020).
• Board member of the Scientific Committee of GDR 2039-CNRS "molecular and cellular aspects of NADPH oxidases " (2019-present).
• Organization of several symposia of the "Oxidase Club" and of the "Neutrophils Club"

Scientific summary

ROS production by NADPH oxidases are important for several biological functions such as signaling and innate immunity. However inappropriate or excessive ROS production by NOX enzymes can disrupt cellular redox equilibrium and damage surrounding tissues, thereby contributing to a wide variety of diseases such as rheumatoid arthritis (RA), inflammatory bowel disease (IBD) and cancer. My research is oriented towards the molecular and cellular mechanisms of inflammation, focusing on the regulation of reactive oxygen species (ROS) production by the NADPH oxidases (NOXs) in phagocytes and other cells such as epithelial cells.

My projects are conducted following three axis: 1) the regulation of NOXs enzymes by pro- and anti-inflammatory agents 2) their role in inflammatory processes by investigating their expression and activation status in human inflammatory diseases and in animal models of inflammation. 3) The identification of new regulators and effectors of NOXs during the inflammatory processes.

Our work have highlighted the key role of phosphorylation/dephosphorylation events in the priming, activation and inactivation of NOX2 in response to inflammatory mediators in phagocytes but also in the activation of NOX1 in epithelial cells. Interestingly in human inflammatory disorders such as rheumatoid arthritis, we have demonstrated a dysregulation of NOX2 which was characterized by its hyperphosphorylation and hyperactivation and developed a pharmacological peptide able to prevent NOX2 hyperactivation without affecting its bactericide functions. On the other hand, we have shown that NOX1 was a key player in mucosal immunity and inflammation by controlling the expression of the innate immune protein, lipocalin-2 (LCN-2).  

Our ultimate goal is to identify novel pharmacological targets for the development of therapeutic tools that will limit the deleterious effects of NOXs in inflammatory disorders.