Tat-CIAPIN1 protein prevents against cytokine-induced cytotoxicity in pancreatic RINm5F β-cells |
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| Authors: | Hyeon Ji Yeo Min Jea Shin Dae Won Kim Hyeok Yil Kwon Won Sik Eum Soo Young Choi |
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| Affiliation: | 1.Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, Korea;2.Department of Biochemistry and Molecular Biology, Research Institute of Oral Sciences, College of Dentistry, Gangneung-Wonju National University, Gangneung 25457, Korea;3.Department of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea |
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| Abstract: | Cytokines activate inflammatory signals and are major mediators in progressive β-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 β-cell damage has not been investigated yet. Thus, we assessed whether the Tat-CIAPIN1 protein can protect RINm5F β-cells against cytokine-induced cytotoxicity. In cytokine-exposed RINm5F β-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-κB 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 β-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 β-cell damage. |
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| Keywords: | Cytokines, Diabetes, MAPK, NF-κ B, Protein therapy, Tat-CIAPIN1 |
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