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Anasuya Sarkar, Ph.D.

Assistant Professor​


Contact Information

Phone: 614-292-1351
Email: Anasuya.Sarkar@osumc.edu


Education

PhD, Indian Institute of Chemical Biology, Jadavpur University, India
Post Doctoral, The Ohio State University


Research Interest

The complexity of the innate host response and its relevance to determining the ultimate response to pathogens and danger signals is the primary focus of my research laboratory. My research interest includes cellular and molecular signaling mechanisms of inflammation in various inflammatory diseases like ARDS/ALI, sepsis, atherosclerosis, cancer with special emphasis on caspase-1 biology. Focused areas include regulation of IL-1beta, NF-kappaB signaling, apoptosis, monocyte and macrophage function and the novel role of microvesicles in regulating these signaling pathways in response to inflammatory infections. Overall, my major focus is on the molecular analysis of signal transduction processes involved in monocyte innate immune responses to microbial pathogens, with a long term goal to identifying molecular targets for therapy of inflammatory diseases.


Current Funded Projects

Microparticulate Caspase-1 mediated lung injury. The proposal seeks to investigate a novel hypothesis that links apoptotic enzyme, caspase-1, encapsulated in circulatory vesicles, to lung cell injury and apoptosis. This proposal provides a much needed effort and framework to study the poorly understood mechanism of endothelial cell injury and vascular dysfunction in ARDS patients and provide new therapeutic opportunities to halt the cell injury in ALI/ARDS patients. This grant is dedicated to understanding the role of microvesicular caspase-1 as modulator of lung endothelium function in Acute Lung Injury. This work will also link clinical samples with fundamental work studying the role of circulating microvesicles as potential mediators of injury.

Microvesicular inflammasomes: role in sepsis. Successful completion of this study will determine if caspase-1 released in submicroscopic packages may interact with target cells to induce their death. Studies outlined here will study the formation and release, as well as cell uptake of these death packages. We expect this approach to uncover novel insights into organ injury of septic patients and thus create new therapeutic opportunities to prevent and treat patients with sepsis and other inflammatory diseases.


Publications​

Sarkar
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