Tat-CIAPIN1 protein prevents against cytokine-induced cytotoxicity in pancreatic RINm5F モ-cells |
Soo Young Choi 1,* (Professor), Hyeon Ji Yeo1 (Ph.D), Min Jea Shin1 (Ph.D), Dae Won Kim (Ph.D), Hyeok Yil Kwon (Professor), Won Sik Eum1 (Ph.D) |
1Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, 2Department of Biochemistry and Molecular Biology, Research Institute of Oral Sciences, College of D, Gangneung-Wonju National University, 3Department of Physiology, College of Medicine, Hallym University |
Abstract
Cytokines activate inflammatory signals and are major mediators in progressive モ-cell damage, which leads to type 1 diabetes mellitus. We recently showed that the cell-permeable Tat-CIAPIN1 fusion protein inhibits neuronal cell death induced by oxidative stress. However, how the Tat- CIAPIN1 protein affects cytokine-induced モ-cell damage has not been investigated yet. Thus, we assessed whether the Tat-CIAPIN1 protein can protect RINm5F モ-cells against cytokine-induced cytotoxicity. In cytokine-exposed RINm5F モ-cells, the transduced Tat-CIAPIN1 protein elevated cell survivals and reduced reactive oxygen species (ROS) and DNA fragmentation levels. The Tat-CIAPIN1 protein reduced mitogen-activated protein kinases (MAPKs) and NF-リB activation levels and elevated Bcl-2 protein, whereas Bax and cleaved Caspase-3 proteins were decreased by this fusion protein. Thus, the protection of RINm5F モ-cells by the Tat-CIAPIN1 protein against cytokine-induced cytotoxicity can suggest that the Tat-CIAPIN1 protein might be used as a therapeutic inhibitor against RINm5F モ-cell damage.
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Abstract, Accepted Manuscript(in press) [Submitted on March 23, 2021, Accepted on April 20, 2021] |
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