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Full NameProfessor Yuri Volkov
Organisation:Trinity College Dublin
Other Research Fields:
Nanomedicine, autoimmune diseases, personalised medicine
Postgrad Medical Specialties
- Occupational Medicine
- Respiratory Medicine
Other Medical Specialties:
Prof. Volkov has expertise in nanomedicine and biomedical applications of nanotechnologies, molecular mechanisms of immune system functioning in health and disease, cell adhesion and migration in inflammation and cancer, intracellular signaling and cytoskeletal dynamics, advanced cell and molecular imaging. Currently his group is pursuing the applications of nanomaterials for advanced research and medical diagnostics and assessment of environmental, health and safety impact of emerging nanomaterials.
Volkov Y. Quantum dots in nanomedicine: recent trends, advances and unresolved issues. Biochem Biophys Res Commun. 2015, 468(3):419-27.
Rakovich TY, Mahfoud OK, Mohamed BM, Prina-Mello A, Crosbie-Staunton K, Van Den Broeck T, De Kimpe L, Sukhanova A, Baty D, Rakovich A, Maier SA, Alves F, Nauwelaers F, Nabiev I, Chames P, Volkov Y. Highly sensitive single domain antibody-quantum dot conjugates for detection of HER2 biomarker in lung and breast cancer cells. ACS Nano. 2014, 8(6):5682-95.
Mohamed BM, Verma NK, Davies AM, McGowan A, Staunton KC,Prina-Mello A, Kelleher D, Botting CH, Causey CP, Thompson PR, Pruijn GJM, Kisin ER, Tkach AV, Shvedova AA, Volkov Y. Citrullination of proteins: a common post-translational modification pathway induced by different nanoparticles in vitro and in vivo. Nanomedicine, 2012, 7(8):1181-95.
Kagan VE, Konduru NV, Feng W, Allen BL, Conroy J, Volkov Y, Vlasova II, Belikova NA, Yanamala N, Kapralov A, Tyurina YY, Shi J, Kisin ER, Murray AR, Franks J, Stolz D, Gou P, Klein-Seetharaman J, Fadeel B, Star A, Shvedova AA. Carbon nanotubes degraded by neutrophil myeloperoxidase induce less pulmonary inflammation. Nat Nanotechnol. 2010, 5(5):354-9.
Williams Y, Sukhanova A, Nowostawska M, Davies AM, Mitchell S, Oleinikov V,Gun'ko Y, Nabiev I, Kelleher D, Volkov Y. Probing cell-type-specific intracellular nanoscale barriers using size-tuned quantum dots. Small. 2009, 5(22):2581-8.
Protein citrullination induced by environmental nanoparticles as a possible pathogenetic link to autoimmune disease development.
Background and hypothesis: Particulate air-pollution or smoking, which has long been considered a non-specific risk factor causing inflammation and general mal-health, has been positively correlated with the risk of autoimmune diseases such as rheumatoid arthritis, multiple sclerosis and psoriasis. Recent studies indicate that such autoimmune conditions are associated with the appearance of citrullinated proteins. Protein citrullination is an enzymatic post-translational modification by the deimination of arginine residues resulting in a loss of positive charge followed by significant biochemical and protein conformational changes. This deformation of proteins exposes amino acid residues that are normally buried in the protein core. The immune system recognizes these newly exposed residues as cryptic epitopes resulting in an autoimmune response in susceptible individuals, with induction of autoreactive antibodies. However, the precise molecular mechanisms by which the environmental ultra-fine particle exposure may contribute to the induction of protein citrullination and subsequent triggering of autoimmune response have not been yet disclosed.
We hypothesize that the airborne nano-sized particles can enter systemic circulation, interact with cellular components and proteins, induce citrullination, and thereby trigger an altered overactive immune response. We believe that this alteration in immune system would contribute to the immune-mediated tissue injury, as observed in rheumatoid arthritis as a chronic inflammatory joint disease.
Experimental: We plan a series of experiments aimed to investigate nanomaterials-induced biological effects, including cellular internalization, intracellular localization, cell-type specificity, and relevant kinetics of nanomaterials in human cells along with proteomic analysis to identify differentially expressed or citrullinated protein(s) in response to nanomaterials. This will be complemented by the investigation of altered signaling pathways, cytokine release and/or activation of specific enzymes in cells exposed to nanomaterials. In parallel, selected relevant patient cohort examination and characterization of samples based on smoking, exposure circumstances etc. to validate the involvement of citrullinated proteins, anti-citrullinated peptides autoantibodies or the identified molecules in immune-mediated tissue injury such as those observed in rheumatoid arthritis will be carried out using the available clinical material.
Expected outcome: The study will provide a molecular explanation for the possible triggering impact of nanomaterials on autoimmune processes development, and suggest molecular target(s) with viable rationale-based therapeutic option(s). The results will be of value for clinicians, immunologists, toxicologists, environmental scientists, and nanotech industries and will contribute to limiting the risk of development and progression of autoimmune diseases.