Korean J Physiol Pharmacol 2012 Dec; 16(6): 463-468
Jong-Sun Yoo1, Yun-Jung Lee1, Kyeong Eun Hyung1, Joo Won Yoon1, Ik Hee Lee1, So-Young Park2, and Kwang Woo Hwang1
Effect of PRX-1 Downregulation in the Type 1 Diabetes Microenvironment
1Laboratory of Host Defense Modulation, College of Pharmacy, Chung-Ang University, Seoul 156-756, 2Department of Pharmacognosy, College of Pharmacy, Dankook University, Chungnam 330-714, Korea
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Type 1 diabetes (T1D) is caused by dysregulation of the immune system in the pancreatic islets, which eventually leads to insulin-producing pancreatic Ղ-cell death and destabilization of glucose homeostasis. One of the major characteristics of T1D pathogenesis is the production of inflammatory mediators by macrophages that result in destruction or damage of pancreatic Ղ-cells. In this study the inflammatory microenvironment of T1D was simulated with RAW264.7 cells and MIN6 cells, acting as macrophages and pancreatic Ղ-cells respectably. In this setting, peroxiredoxin-1, an anti-oxidant enzyme was knocked down to observe its functions in the pathogenesis of T1D. RAW264.7 cells were primed with lipopolysaccharide and co-cultured with MIN6 cells while PRX-1 was knocked down in one or both cell types. Our results suggest that hindrance of PRX-1 activity or the deficiency of this enzyme in inflammatory conditions negatively affects pancreatic Ղ-cell survival. The observed decrease in viability of MIN6 cells seems to be caused by nitric oxide production. Additionally, it seems that PRX-1 affects previously reported protective activity of IL-6 in pancreatic Ղ cells as well. These results signify new, undiscovered roles for PRX-1 in inflammatory conditions and may contribute toward our understanding of autoimmunity.
Keyword : Nitric oxide, Pancreatic Ղ-cell, Peroxiredoxin, Type 1 diabetes

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