Effect of PRX-1 Downregulation in the Type 1 Diabetes Microenvironment.
10.4196/kjpp.2012.16.6.463
- Author:
Jong Sun YOO
1
;
Yun Jung LEE
;
Kyeong Eun HYUNG
;
Joo Won YOON
;
Ik Hee LEE
;
So Young PARK
;
Kwang Woo HWANG
Author Information
1. Laboratory of Host Defense Modulation, College of Pharmacy, Chung-Ang University, Seoul 156-756, Korea. khwang@cau.ac.kr
- Publication Type:Original Article
- Keywords:
Nitric oxide;
Pancreatic beta-cell;
Peroxiredoxin;
Type 1 diabetes
- MeSH:
Autoimmunity;
Down-Regulation;
Glucose;
Homeostasis;
Immune System;
Insulin-Secreting Cells;
Interleukin-6;
Islets of Langerhans;
Macrophages;
Nitric Oxide;
Peroxiredoxins
- From:The Korean Journal of Physiology and Pharmacology
2012;16(6):463-468
- CountryRepublic of Korea
- Language:English
-
Abstract:
Type 1 diabetes (T1D) is caused by dysregulation of the immune system in the pancreatic islets, which eventually leads to insulin-producing pancreatic beta-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 beta-cells. In this study the inflammatory microenvironment of T1D was simulated with RAW264.7 cells and MIN6 cells, acting as macrophages and pancreatic beta-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 beta-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 beta cells as well. These results signify new, undiscovered roles for PRX-1 in inflammatory conditions and may contribute toward our understanding of autoimmunity.
