Sandra Costa

  • lung
  • fibrosis
  • acute injury
  • differentiation
  • repair regeneration
  • macrophages

I graduated in Applied Biology from the School of Sciences, the University of Minho in 2000, completed an MSc degree in Oncology from ICBAS, the University of Porto in 2003, and obtained a Ph.D. degree in Health Sciences, Biological and Biomedical scientific area from the School of Medicine, the University of Minho in 2007. During my post-doc in Massimiliano Mazzone’s lab (at CCB, VIB-KU Leuven, Belgium), I explored mechanisms wherein the skewing of macrophage polarization decisively dictated the outcome of ischemic diseases and cancer. In addition, I addressed the role of specific molecules in inflammatory cells in driving lung cancer. In 2015, I started my lab. Our research goals include unveiling key cellular and molecular players in lung development and injury. We are manipulating iPSC-derived macrophages to secrete potential mediators of interest to intensify lung maturity and regeneration. With this, I foresaw bringing new cell-free therapeutic strategies for pediatric and adult lung chronic diseases applications. Moreover, we investigate molecular modulation of the immune system and signaling pathways underlying epithelial‐immune-stroma crosstalk in lung acute injury and fibrosis progression. We apply various technical approaches in lung biology and immunology fields, such as primary mouse lung epithelial/immune cell cultures, iPSC-derived macrophages, and lung epithelial cell organoids generation, 3-D ex vivo fetal and adult lung cultures, and acute lung injury and pulmonary fibrosis disease mouse models.

Scientific Highlights

* “Macrophage-secreted mediators as therapeutic strategy for preterm lung maturation”, scientific research project funded by FEDER, through the Competitiveness Internationalization Operational Programme (POCI), and by National funds, through the Foundation for Science and Technology (FCT), Principal Investigator, 2018-2022. *“Unravelling the key roles of tissue macrophages in lung morphogenesis and injury”, Exploratory Project grant within FCT Investigator program from FCT, reference IF/00959/2014; Principal Investigator, 2015-2020. *Finisguerra V, Di Conza G, Di Matteo M, Serneels J, Costa S, Thompson R, Wauters E, Walmsley S, Prenen H, Granot Z, Casazza A, Mazzone M. MET is required for the recruitment of anti-tumoural neutrophils. Nature, 2015; 522(7556):349-53. *Hamm A, Veschini L, Takeda Y, Costa S, Delamarre E, Squadrito ML, Henze A-T, Wenes M, Serneels J, Pucci F, Roncal C, Anisimov A, Alitalo K, DePalma M, Mazzone M. PHD2 regulates arteriogenic macrophages through TIE2 signaling. EMBO Mol Med (2013); 5(6):843-57. *Takeda Y, Costa S, Delamarre E, Roncal C, Leite De Oliveira R, Squadrito ML, Finisguerra V, Deschoemaeker S, Bruyère F, Wenes M, Hamm A, Serneels J, Magat J, Bhattacharyya T, Anisimov A, Jordan BF, Alitalo K, Maxwell P, Gallez B, Zhuang ZW, Saito Y, Simons M, De Palma M, Mazzone M. Macrophage skewing by Phd2 haplodeficiency prevents ischaemia by inducing arteriogenesis. Nature (2011); 479(7371): 122-126.