Laura Nagy, Ph.D.

Staff

Lerner Research Institute, 9500 Euclid Avenue, Cleveland, Ohio 44195
Location: NE4-207
Email: nagyl3@ccf.org
Phone: (216) 444-4021
Fax: (216) 636-1493

 


The research in my laboratory is aimed at understanding how chronic alcohol consumption contributes to chronic diseases, such as liver disease and diabetes. Recent data indicate that alcoholic liver disease affects over 10 million Americans and chronic, heavy alcohol consumption is an independent risk factor for type 2 diabetes. We’ve been particularly involved in understanding the effects of ethanol on hormone and cytokine receptor-dependent signal transduction. It has been our working hypothesis that disruption of signalling by hormones and cytokines contributes to the development of specific pathologies associated with chronic alcohol consumption Several projects in the laboratory address the pathophysiological mechanisms of ethanol-induced liver injury. In particular, we are interested in the contributions of the innate immune system, including the resident macrophage in the liver (Kupffer cells) and the complement pathway, in the initiation and progression of ethanol-induced liver injury. Recent work in the laboratory has also implicated ethanol-induced changes in adipose tissue metabolism and regulatory activity as a contributor to ethanol-induced insulin resistance and liver injury. Making use of cell and animal models, my laboratory group addresses some of the fundamental questions of how ethanol exposure injures the liver, with a goal ofidentifying the individual targets of ethanol-induced injury and the specific responses of the key cell types within the liver, as well as the integrated, organismal response to this ethanol-induced injury.

In other words ...

The research in my laboratory is aimed at understanding how chronic alcohol consumption contributes to chronic diseases, such as liver disease and diabetes. Recent data indicate that alcoholic liver disease affects over 10 million Americans and chronic, heavy alcohol consumption is an independent risk factor for type 2 diabetes. Making use of cell and animal models, my laboratory group addresses some of the fundamental questions of how ethanol exposure injures the liver, with a goal of identifying the individual targets of ethanol-induced injury and the specific responses of the key cell types within the liver, as well as the integrated, organismal response to this ethanol-induced injury.


Doug  Czarnecki  Doug Czarnecki
Animal Husbandry Technician
Location:NE4-214
Phone:(216) 444-8632
czarned@ccf.org
Xiude  Fan  Xiude Fan
Predoctoral Fellow
Location:NE4-214
Phone:(216) 444-8632
fanx@ccf.org
Christopher  Kibler  BA Christopher Kibler, BA
Research Technician
Location:NE4-214
Phone:(216) 444-8632
kiblerc@ccf.org
Adam  Kim  PhD Adam Kim, PhD
Postdoctoral Fellow
Location:NE4-214
Phone:(216) 444-8632
kima7@ccf.org
Megan  McMullen  Megan McMullen
Project Manager
Location:NE4-214
Phone:(216) 444-8632
mcmullm2@ccf.org
Kyle  Poulsen  PhD Kyle Poulsen, PhD
Postdoctoral Research Fellow
Location:NE4-214
Phone:(216) 444-8632
poulsek@ccf.org
Carlos  Sanz Garcia  PhD Carlos Sanz Garcia, PhD
Postdoctoral Research Fellow
Location:NE4-214
Phone:(216) 444-8632
sanzc@ccf.org
Dhara  Sharma  PhD Dhara Sharma, PhD
Postdoctoral Fellow
Location:NE4-214
Phone:(216) 444-8632
sharmad2@ccf.org
Jeanette  Wat  Jeanette Wat
Location:NE4-214
Phone:(216) 444-8632
watj@ccf.org
Xiaoqin  Wu  PhD Xiaoqin Wu, PhD
Postdoctoral Fellow
Location:NE4-215
Phone:(530) 220-5084
wux@ccf.org

Myeloid-Mixed Lineage Kinase 3 contributes to chronic ethanol-induced inflammation and hepatocyte injury in mice.

McCullough RL, Saikia P, Pollard KA, McMullen MR, Nagy LE, Roychowdhury S.

Gene Expr. 2016 Jun 9. [Epub ahead of print]

 

Receptor interacting protein 3 protects mice from high fat diet-induced liver injury.

Roychowdhury S, McCullough RL, Sanz-Garcia C, Saikia P, Alkhouri N, Matloob A, Pollard K, McMullen MR, Croniger CM, Nagy LE.

Hepatology. 2016 Jun 15. doi: 10.1002/hep.28676. [Epub ahead of print]

 

Differential contribution of complement receptor C5aR in myeloid and non-myeloid cells in chronic ethanol-induced liver injury in mice.

McCullough RL, McMullen MR, Das D, Roychowdhury S, Strainic MG, Medof ME, Nagy LE.

Mol Immunol. 2016 Jul;75:122-32. doi: 10.1016/j.molimm.2016.05.006. Epub 2016 Jun 6.

 

Soluble IgM links apoptosis to complement activation in early alcoholic liver disease in mice.

Smathers RL, Chiang DJ, McMullen MR, Feldstein AE, Roychowdhury S, Nagy LE.

Mol Immunol. 2016 Apr;72:9-18. doi: 10.1016/j.molimm.2016.02.008. Epub 2016 Feb 27.

 

Linking Pathogenic Mechanisms of Alcoholic Liver Disease With Clinical Phenotypes.

Nagy LE, Ding WX, Cresci G, Saikia P, Shah VH.

Gastroenterology. 2016 Jun;150(8):1756-68. doi: 10.1053/j.gastro.2016.02.035. Epub 2016 Feb 23.

 

Adiponectin as an anti-fibrotic and anti-inflammatory adipokine in the liver.

Park PH, Sanz-Garcia C, Nagy LE.

Curr Pathobiol Rep. 2015 Dec 1;3(4):243-252. Epub 2015 Sep 30.

 

The Role of Innate Immunity in Alcoholic Liver Disease.

Nagy LE.

Alcohol Res. 2015;37(2):237-50. Review.

 

Alternative complement pathway component Factor D contributes to efficient clearance of tissue debris following acute CCl₄-induced injury.

Cresci GA, Allende D, McMullen MR, Nagy LE.

Mol Immunol. 2015 Mar;64(1):9-17. doi: 10.1016/j.molimm.2014.10.017. Epub 2014 Nov 15.

 

Macrophage migration inhibitory factor is required for recruitment of scar-associated macrophages during liver fibrosis.

Barnes MA, McMullen MR, Roychowdhury S, Madhun NZ, Niese K, Olman MA, Stavitsky AB, Bucala R, Nagy LE.

J Leukoc Biol. 2015 Jan;97(1):161-9. doi: 10.1189/jlb.3A0614-280R. Epub 2014 Nov 14.

 

Innate immunity and cell death in alcoholic liver disease: role of cytochrome P4502E1.

Barnes MA, Roychowdhury S, Nagy LE.

Redox Biol. 2014 Aug 1;2:929-35. doi: 10.1016/j.redox.2014.07.007. eCollection 2014. Review.


07/03/2018 |  

New LRI Co-Laboratories Announced

A new internally funded award, called the Co-Laboratories Award, encourages new, "start-up" collaborations that bring together researchers from different laboratories to investigate and attack disease from many angles, drawing on the unique expertise and innovations that each laboratory has to offer. The award provides a total of $100,000 in project funding over the course of two years. In its inaugural year, the award funded two exciting cross-disciplinary projects that will investigate neuronal dysfunction in alcohol abuse and smooth muscle hyperplasia in Crohn's disease.