Alla Mitrofanova, Ph.D.

Roles

• Biography

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  During my years as a student and postdoctoral fellow, I have developed a solid background in multiple disciplines, including physiology, cell and molecular biology, biochemistry, genetics, along with very broad technical skills, including unique techniques of surgical manipulations with rodents, glomeruli isolation and podocyte primary cell culture. In the laboratory, I have been working with several experimental in vivo models of diabetes and glomerulosclerosis with a primary focus on metabolic pathways that modulates the function of glomerular cells (podocytes), with a primary interest in insulin signaling, innate immune system and lipid/sphingolipid metabolism. During my graduate student time, I was awarded the personal Graduate Student Grant twice. At the Laboratory of Receptor Cell Biology (Moscow, Russia), I have expanded my scientific view and obtained new experience in the molecular biology field by working on the study of insulin receptor-related receptor structure and function in kidneys. As a postdoctoral fellow at the laboratory of Dr. Fornoni, I had been particularly interested to study how sphingolipids affect insulin signaling in podocytes leading to development of DKD. I was able to discover that sphingomyelin phosphodiesterase acid-like 3b may affect availability of biologically active sphingolipids, such as ceramide-1-phosphate, contributing to development of DKD. In another project, I have also uncovered how cholesterol esters contribute to the progression of the glomerular disease in the experimental Alport syndrome, a murine model of FSGS. Overall, during my postdoctoral fellow time at the University of Miami, I contributed to the generation of fourteen peer-reviewed publications.

• Education & Training

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  Education

  2011: Saint Petersburg State University, Saint Petersburg, Russia

  PhD

• Research Interests

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  My current research focus is related to the contribution of innate immunity in the pathogenesis of glomerular diseases. Using basic science approach, my project elucidates the role of stimulator of interferon genes (STING) in the development and progression of diabetic kidney disease and focal segmental glomerulosclerosis using various mouse models, cell-based assays and human samples. We were able to show that STING activity is upregulated in human podocytes treated with sera of patients with diabetic kidney disease and in glomeruli from mouse models of diabetic kidney disease. Interestingly, the activation of STING alone results in impaired renal function in wildtype mice, while pharmacological inhibition of STING ameliorates kidney injury in diabetic mice. However, it is not known what the mechanism is leading to STING activation in glomerular diseases. We know that cytosolic leakage of mitochondrial DNA (mtDNA) contributes to inflammation and fibrosis in kidney disease and was shown to interact with cyclic GMP-AMP synthase and STING, a pathway that may also contribute to the pathogenesis of diabetic kidney disease. If mtDNA contributes to podocyte injury in diabetic kidney disease and focal segmental glomerulosclerosis and what are the mechanisms leading to the cytosol mtDNA leakage remain unclear. The overarching long-term goal of my research is to understand the molecular mechanisms leading to STING constitutive activation and chronic sterile inflammation in conditions of diabetic kidney disease and focal segmental glomerulosclerosis, which will open new therapeutic opportunities to treat glomerular diseases.

• Publications

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