CV Science

Giulia Chinetti PhD in pharamceutical technologies

Course and current status

2010:Team leader (Team 2, Inserm U1011)

2009: Research Director INSERM

2002: Senior scientist INSERM

2002: Authorization to supervise research (Faculté de Pharmacie; Université de Lille - France)

1996: Authorization to work as pharmacist (Faculty of Pharmacy; University of Milan)

1995: Thesis in Chemistry and Pharmaceutical Sciences (Faculty of Pharmacy; University of Milan)

Scientific summary

Monocyte derived-macrophages are central cells in the development of metabolic disorders and related diseases such as obesity and atherosclerosis, since they can infiltrate adipose tissue as well as the vascular wall, respectively, contributing to the maintenance of an inflammatory status. However, two different sub-populations of macrophages have been identified in adipose tissue and atherosclerotic lesions: pro-inflammatory “classical” M1 and anti-inflammatory “alternative” M2 macrophages, and their ratio is suggested to play a role in the metabolic complications of obesity. On the other hand, it is thought that adipose tissue products may, in turn, modulate peripheral blood mononuclear cells (PBMC) and monocyte functions.

During the past few years we focused our investigations on the effects of PPAR and LXR activation on circulating monocyte-derived macrophages, with particular emphasis on their role on modulation of lipid homeostasis and inflammation.

In our current research project, the general objective is to understand the consequences of obesity and its comorbidities on monocyte functions and to study their modulation by PPARg. In a second attempt, we will be interested by the study of molecular regulation of monocyte macrophage differentiation and functions of classical or alternative macrophage infiltrating atherosclerotic plaques and adipose tissue by PPAR and LXR  as well as the consequences of their cross-talk.

To get further inside into the role of these factors in regulation of monocyte/macrophage functions, human materials (blood cells, adipose tissue and atherosclerotic plaques) will be analyzed. Laser capture micro-dissection, histology, cellular biology and biochemical approaches will be used. Concomitantly, molecular biology methods (quantitive PCR, western blot, DNA-microarray and ChIP seq) will be combined to delineate the molecular mechanisms at the basis of the identified functions.