IL-32 gamma overexpression accelerates streptozotocin (STZ)-induced type 1 diabetes
- Authors
- Jhun, Hyunjhung; Choi, Jida; Hong, Jaewoo; Lee, Siyoung; Kwak, Areum; Kim, Eunsom; Jo, Seunghyun; Ryoo, Soyoon; Lim, Yoojung; Yoon, Do-Young; Hong, Jin Tae; Kim, Tae Sung; Lee, Youngmin; Song, Keeho; Kim, Soohyun
- Issue Date
- 9월-2014
- Publisher
- ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
- Keywords
- IL-32 gamma transgenic mice; Inflammatory cytokine; Streptozotocin (STZ)-induced type I diabetes; Pancreas; Glucose tolerance test
- Citation
- CYTOKINE, v.69, no.1, pp.1 - 5
- Indexed
- SCIE
SCOPUS
- Journal Title
- CYTOKINE
- Volume
- 69
- Number
- 1
- Start Page
- 1
- End Page
- 5
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/97532
- DOI
- 10.1016/j.cyto.2014.05.002
- ISSN
- 1043-4666
- Abstract
- Interleukin-32 (IL-32) is a cytokine produced by T lymphocytes, natural killer (NK) cells, monocytes and epithelial cells. There are five splicing variants (alpha, beta, gamma, delta, and epsilon) and IL-32 gamma is the most active isoform. We generated human IL-32 gamma transgenic (IL-32 gamma TG) mice, displaying a high level of IL-32 gamma expression in the pancreas. We investigated the effect of IL-32 gamma on streptozotocin (STZ)-induced type I diabetes model using IL-32 gamma TG mice. After a suboptimal diabetogenic dose of STZ administration, IL-32 gamma TG mice showed significantly increased blood glucose level comparing with that of wild type (WT) mice at day 5. Inflammatory cytokines levels such as, IL-6, TNF alpha, IFN gamma and IL-1 beta, in pancreas and liver lysates were accessed by a specific cytokine ELISA. The proinflammatory cytokines were significantly enhanced in the pancreas of IL-32 gamma TG mice comparing to that of WT mice whereas those cytokines levels in liver of IL-32 gamma TG and WT mice were not changed by STZ. These data indicate that the overexpression of IL-32 gamma contributes to initial islet beta-cells injury and inflammation in pancreas and aggravates STZ-induced type 1 diabetes. (C) 2014 Elsevier Ltd. All rights reserved.
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