Mateos Martín

Professional Category: Postdoc Researcher
Academic History: Degree in Biology
CSIC Scientific Areas: Food Science and Technology

Lines of Research:

-Gene cloning and gene expression. Lentiviral transduction of cells. Real Time PCR. RNAseq

-Protein purification (Sephadex, Silica) Protein separation and isolation (PAGE, IEF),Liquid Chromatography

-Mass Spectrometry: ABSciex 4800 TOF/TOF; ABSciex 5500 Q-Trap; Thermo LTQ-Orbitrap Elite). Quantitative proteomics (iTRAQ, SILAC, Label-free, TMT10plex, MRM).

-Serum endogenous Peptide separation by Solid Phase Extraction andde novo sequencing

-Cell and tissue culture. Isolation of Mesenchymal Stem Cells of different origins (umbilical cord stroma, synovial membrane, bone marrow). Directed differentiation of stem cells to adipocytes, bone, chondrocytes, etc, optical microscopy, confocal microscopy. Immunoblotting and ELISA

-Handling of clinical samples (plasma, serum, saliva, sputum and cartilage).

-Data and statistical analysis. Software skills: 4000 Series explorer, Protein Pilot, MaxQuant, Mascot, Peaks, Analyst, TPP, Proteome Discoverer, Multiquant, MRMPilot, Skyline,  R, Prisma, SPSS

Free CV summary/biography:

Over the past years I have developed extensive training in Proteomics applied to the study of human diseases On one hand I have perfected the use and management of proteomic platforms that have allowed the determination of differential protein profile of human synovial fluid between two degenerative diseases affecting the joint, but with different molecular origins, Osteoarthritis (OA) and Rheumatoid arthritis (RA) (Mateos et al, 2012, 2014, 2017). The main conclusion of this study lies in the fact that it is possible to differentiate the synovial fluid of these two diseases in terms of their protein content. While in the case of synovial fluid from osteoarthritic patients (OA) proteins involved in the synthesis and structure of the extracellular matrix (ECM) of the cartilage are more abundant, in Rheumatoid Arthritis (RA) there is an accumulation of components involved in the inflammation process and immune response. On the other hand I have studied the molecular mechanisms of OA and premature aging (Progeria Syndrome) due to the deregulation of the expression of the nuclear protein Lamin A (Mateos et al 2013, 2015). I focused on the effect of over-expression in mesenchymal stem cells (MSCs) of Lamin A or a mutated isoform call Progerin (PG), which causes the genetic syndrome Progeria (HGPS). This is a currently incurable disease characterized by a recapitulation, at very early age, of classic symptoms of aging, including arthritis and lipodystrophy. The deregulation of the Lamina A causes in these cells defects in their chondrogenic capacity. We have shown that these defects are due in part to an accumulation of Reactive Oxygen Species (ROS). Since May, 2016 I have a postdoctoral position at the Spanish Research Council (CSIC) working on the EMI-TB (Eliciting Mucosal Immunity in Tuberculosis) consortium, an EU Horizon2020 funded action focused on selecting and developing a novel vaccine candidate for Tuberculosis.