Articles by Isabelle Maridonneau-Parini in JoVE
Protrusion Force Microscopy: A Method to Quantify Forces Developed by Cell Protrusions Anaïs Bouissou*1, Amsha Proag*1, Marion Portes1, Vanessa Soldan2, Stéphanie Balor2, Christophe Thibault3,4, Christophe Vieu3,4, Isabelle Maridonneau-Parini1, Renaud Poincloux1 1Institut de Pharmacologie et Biologie Structurale, IPBS, Université de Toulouse, CNRS, UPS, 2METi, 3CNRS, LAAS, 4Univ de Toulouse, INSA Here, we detail the experimental techniques used to evaluate the protrusion forces that podosomes apply on a compliant film, from the preparation of the film to the automated analysis of topographical images.
Other articles by Isabelle Maridonneau-Parini on PubMed
Bone Degradation Machinery of Osteoclasts: An HIV-1 Target That Contributes to Bone Loss Proceedings of the National Academy of Sciences of the United States of America. Mar, 2018 | Pubmed ID: 29463701 Bone deficits are frequent in HIV-1-infected patients. We report here that osteoclasts, the cells specialized in bone resorption, are infected by HIV-1 in vivo in humanized mice and ex vivo in human joint biopsies. In vitro, infection of human osteoclasts occurs at different stages of osteoclastogenesis via cell-free viruses and, more efficiently, by transfer from infected T cells. HIV-1 infection markedly enhances adhesion and osteolytic activity of human osteoclasts by modifying the structure and function of the sealing zone, the osteoclast-specific bone degradation machinery. Indeed, the sealing zone is broader due to F-actin enrichment of its basal units (i.e., the podosomes). The viral protein Nef is involved in all HIV-1-induced effects partly through the activation of Src, a regulator of podosomes and of their assembly as a sealing zone. Supporting these results, Nef-transgenic mice exhibit an increased osteoclast density and bone defects, and osteoclasts derived from these animals display high osteolytic activity. Altogether, our study evidences osteoclasts as host cells for HIV-1 and their pathological contribution to bone disorders induced by this virus, in part via Nef.