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Pranoti Mandrekar, Ph.D.

 

Other Affiliation(s):

Director, Translational Science Program
Director, NIH Summer Research Program

Graduate School of Biomedical Sciences

 

STRESS RESPONSES AND PROTEOSTASIS REGULATORS IN LIVER INFLAMMATION ANND FIBROSIS

Research in my laboratory focuses on understanding the signaling mechanisms involved in innate immune cell activation during liver injury and cancer. The physiological function of the liver is elimination of pathogens and antigens from the blood for which mounting of an immune response is required. To avoid unnecessary activation of the immune system, the liver develops a local immune response followed by induction of peripheral tolerance towards the antigen. When stressful agents such as pathogens or environmental insults challenge the liver for extended periods of time and their elimination is not possible, inflammation and injury follows. The onset of inflammation in the liver is followed by fibrosis, cirrhosis and liver cancer. Thus, studying the mechanisms involved in liver inflammation will provide major insights into pathogenesis of liver disease and progression.

Using various in vivo and in vitro models, we are studying the role of innate immune signaling pathways, their crosstalk with oxidative stress mechanisms leading to pro-inflammatory cytokine production. We are also focusing on investigating the role of chemokine responses and their effect on recruitment of bone-marrow derived cells and immune cells in the liver during development and progression of liver disease. Recent studies initiated in our lab focus on the impact of alcohol drinking on breast and liver cancer. Th main areas of focus are:

1) Proteostasis mechanisms in fatty liver disease, inflammation and fibrosis

Characterization of an interplay of immune and oxidative stress related mechanisms involved in mediating the effects of acute and chronic alcohol consumption, and epigenetic pathways altered in chronic liver diseases using alcoholic and non-alcoholic liver disease models are being studied. We identified a pathogenic role for stress mediated transcription factor HSF1 and its target gene, hsp90 and hsp70 in innate immune cells resulting in regulation of inflammatory responses. Using molecular and targeted translational approaches we are currently evaluating hsp90 and hsp70 as a therapeutic targets in manipulation of macrophage function in host defense and liver diseases such as alcoholic liver disease and fibrosis.

2) Gut-liver-brain Axis in Liver Diseases

The impact of

3) Adipose-Liver Crosstalk

 

4) Chemokines and importance of immune liver cell types in liver injury

The dynamic role of immune cells and bone marrow derived hematopoietic cells and their cross talk with other liver cell types in promoting liver diseases is being investigated. Liver macrophages, dendritic cells, NK and NKT cells play an important function in development and progression of liver disease. We propose to unravel the role of chemokinesin recruitment of immune cells in the liver and modulate chronic liver injury. Specifically, studies from our laboratory have identified a significant role for a CC-chemokine, monocyte chemoattractant protein -1 (MCP-1) in induction of fatty liver disease. We hypothesize that CCL2 is an important link between innate immune mechanisms and steatosis or fatty liver. Other chemokines and chemokine receptors are also being explored to determine the role of MCP-1 in mediating inflammatory processes leading to alcoholic liver injury.

 

 

 


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  • Receptors Chemokine