دكتورة/نوف بنت محمد الرشيد

I gained experience in a number of pharmacological and biochemical approaches to examining cellular signaling events and exocytosis. In particular, I gained experience in immunoblotting and immunocytochemistry; confocal microscopy; live cell imaging of single-cell signaling events using Ca2+-sensitive dyes and eGFP-tagged proteins; population-based measurements of phosphoinositide signaling; cell culture of established cell lines; preparation and culture of primary cells; handling of cDNA; determination of catecholamine release from cell populations; animal models of various diseases related to, in particular, behavioral studies of major depressive disorders, especially models of treatment-resistant depression; and cardiovascular disease models such myocardial infarction models, cardiac hypertrophy, and hypertensive models. Among all these models, most of my attention is directed to animal models of diabetes—particularly type 2 diabetes mellitus complications—focusing on the methods of induction, characterization, and biomarkers in animal models of both diabetic cardiomyopathy and diabetic nephropathy.

My professional interests primarily focus on cell signaling, particularly G-protein coupled receptors (GPCRs)-mediated intracellular calcium signaling and its impact on neurotransmitter release, since the modulation of neurotransmitter release by ionotropic nicotinic receptors and Gaq/11-coupled receptors may be essential for events such as the regulation of cardiovascular function and stress response—a major focus of my research. The role of specific protein kinase C (PKC) isoforms in regulating neurotransmitter release triggered by nicotinic receptor activation and the mechanisms underlying PKC activation and its regulation of exocytosis. Second, signaling pathways are involved in the pathophysiology of diabetes and diabetic complications, such as cardiovascular and diabetic nephropathy complications, especially the involvement of inflammatory pathways and the immune system in the pathophysiology of such diseases. Currently, my collaborative research group and I pay attention to studying the role of macrophage depletion, the JAK/STAT signaling pathway, fatty acid binding protein 4 (FABP4), angiopoietin-like protein 2 (AGPTL2), G-protein-coupled kinase 2 (GRK2), growth differentiation factor-15 (GDF-15), and age-associated diseases such as senescence, as all these interested molecular targets could be future promising targets for the development of drugs that might play protective and preventive roles against the development of diabetic complications.