ResearchGate 

ORCID

katarina.mihajlovic@bio.bg.ac.rs

Katarina Mihajlović, MSc

Research Trainee, Ph.D. student, Department of General Physiology and Biophysics, Faculty of Biology University of Belgrade, Studentski trg 3, 11001 Belgrade, Serbia

In our brainpurinergic world, my research focus is on enzyme ecto-5 nucleosidase (eN/CD73). The increase in both activity and expression of CD73 is noticed in brain pathological conditions, contributing to chronic neuroinflammation. My PhD experiments are part of a preclinical study where I am testing novel CD73- targeting inhibitors on rat astrocytes in vitro hoping that one day they can be used in humans for treating chronic neuroinflammation that is characteristic of all neurodegenerative diseases.

ResearchGate

ORCID

andjela.stekic@bio.bg.ac.rs

Anđela Stekić, MSc

Research Trainee, Ph.D. student, Department of General Physiology and Biophysics, Faculty of Biology University of Belgrade, Studentski trg 3, 11001 Belgrade, Serbia

I am a researcher interested in purinergic signaling in physiological and pathophysiological processes occurring in central nervous system. My PhD research field is adenosine deaminase and other enzymes/receptors involved in purinergic signaling, especially in olfactory bulb and hypothalamus and their role in neuroinflammation, in animal model of multiple sclerosis - experimental autoimmune encephalomyelitis (EAE).  

ResearchGate

ORCID

milica.zeljkovic@bio.bg.ac.rs

Milica Zeljković Jovanović, MSc

Research assistant, Ph.D. student, Department of General Physiology and Biophysics, Faculty of Biology University of Belgrade, Studentski trg 3, 11001 Belgrade, Serbia

Milica Zeljković is a researcher interested in purinergic signaling in neurodegenerative disorders. Her Ph.D. research is focused on changes in activity and expression of enzymes/receptors involved in purinergic signaling, especially their role in neuroinflammation, in an animal model of Parkinson’s diseases after treatment with repetitive transcranial magnetic stimulation (rTMS), a non-invasive and painless stimulation protocol which modulates excitability and activity of stimulated brain area.  She is skilled in a variety of laboratory techniques including oxidative stress analysis, Western blot, ELISAs, and immunohistochemistry analysis. 

ResearchGate
ORCID

amarija@bio.bg.ac.rs

Marija Adžić Bukvić, Ph.D.

Resarch Asociate, Department of General Physiology and Biophysics, Faculty of Biology University of Belgrade, Studentski trg 3, 11001 Belgrade, Serbia

My research focuse is membrane-bound ectoenzyme, ecto-5’-nucleotidase (eN/CD73) which balances extracellular purines concentrations, and, may be said, controls purinergic signaling. This enzyme hydrolyzes AMP to adenosine, thus, shifting the signaling pathways from P2 to P1 purinergic receptors, consequently potentiating adenosine signaling actions. Ecto-5’-nucleotidases is known to function as a cellular adhesion molecule (CAM), as well, and is engaged in direct interactions with ECM, such as tenascin C, laminin or fibronectin. It is special interest of my research to investigate both roles of CD73 and their significance, impact on cellular behavior and participation in inflammatory processes altogether. In the context of neuroinflammation, reactive astrocytes undergo drastic changes, obtaining either beneficiary or malevolent characteristics, modifying their morphology, migratory capacity and transcriptome set including the incensement of CD73. Since it has already been recognized as antibody treatment target in cancer biology, my interest is turned towards unveiling both of this protein’s roles, as enzyme and as adhesion molecule, and its potencies to be pharmacologically manipulated in favor of neuroinflammation resolution in CNS pathologies.

ResearchGate
ORCID
milorad.dragic@bio.bg.ac.rs

Milorad Dragić, Ph.D.

Teaching Assistant, Department of General Physiology and Biophysics, Faculty of Biology University of Belgrade, Studentski trg 3, 11001 Belgrade, Serbia

Milorad Dragić is a young, enthusiastic researcher with interest in purinergic signalling in neurodegenerative disorders. His PhD research is focused on changes in both, activity and expression of hippocampal ecto-5ˈ nucleotidase, NTPDase 1 and NTPDase 2 in trimethyltin-induced neurodegenration, an animal model of Alzheimer-like disease. Trimethyltin is neurotoxic substance specifically affecting hippocampal formation, causing neuronal death, neuroinflammation, activation of microglia and astrocyte without disruption of blood-brain barrier.

ResearchGate
ORCID
danijela@bio.bg.ac.rs

Danijela Laketa, Ph.D.

Associate Professor, Department of General Physiology and Biophysics, Faculty of Biology University of Belgrade, Studentski trg 3, 11001 Belgrade, Serbia

My research field is the complex interplay between major ectonucleotidases in the CNS, i.e. NTPDase1/CD39, NTPDase2 and e-5NT/CD73 in neuroinflammatory conditions. The ratio between NTPDase1/CD73 activity determines the extracellular levels of adenosine and ATP, which crucially affect the tissue inflammatory status. We have recently demonstrated induction of NTPDase1/CD39 and e-5NT/CD73 in experimental autoimmune encephalomyelitis/EAE. Massive up-regulation of the ectonucleotidases chain during EAE results in faster elimination of ATP and ADP, which are the ligands for P2 receptors, and accumulation of  adenosine, which acts at P1 receptor subtypes. The shift in ATP/adenosine ratio potentiates anti-inflammatory effects and promotes resolution of neuroinflammation. We have also demonstrated significant change in P2 and P1 receptor expression during EAE.   

ResearchGate
ORCID
nnedel@bio.bg.ac.rs

Nadežda Nedeljković Ph.D.

Full Professor, Department of General Physiology and Biophysics, Faculty of Biology University of Belgrade, Studentski trg 3, 11001 Belgrade, Serbia

Study of a complex role of ecto-5'-nucleotidase/CD73 and possibility of using CD73/A2AR axis as a therapeutic target in chronic neuroinflammatory diseases. A number of novel CD73-targeting drugs, competitive and noncompetitive inhibitors and monoclonal antibodies have been developed in recent years, due to growing evidence linking the CD73 with cancer progression and immune escape. Our group is testing these novel CD73 inhibitors for their potency to suppress the inflammatory response and to ameliorate neurological deficits in chronic neuroinflammatory conditions.