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This galley proof is being listed electronically before publishing the final manuscript (It's not final version).

 
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.
Abstract, Accepted Manuscript(in press) [Submitted on March 23, 2021, Accepted on April 20, 2021]
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