Our laboratory is interested in how oxidative stress is related to the onset and/or progression of various diseases including diabetes, atherosclerosis and neurodegenerative disorders. Oxygen is essential for prokaryotic and eukaryotic cells to obtain energy. However, reactive oxygen species (ROS) are generated as by-products of cellular metabolism of oxygen even under normal physiological conditions. These molecules are high reactive and cause oxidative damage to cellular components, resulting in cytotoxicity. To avoid oxidative damage, cells have the antioxidative defense systems such as antioxidants and enzymes generate ROS scavenging activity, such as superoxide dismutase (SOD). Oxidative stress is caused by an imbalance between production of ROS and the antioxidative defense systems. On the other hand, however, recent reports have demonstrated that ROS serve as signaling molecules for altering the redox state of specific target molecules that affect cellular functions. Our current works focus on redox regulation of cell signaling under pathological conditions and epigenetic regulation of gene expression of anti-oxidative enzymes.
研究課題 Research Objectives
脳内微量金属の恒常性破綻による神経細胞障害の分子機構 Mechanisms of cerebral metal imbalance-related neuronal dysfunction
がん微小環境におけるレドックス関連タンパクの機能の解明 Regulation of redox-related proteins in tumor microenvironment
大気圧プラズマによる細胞応答の分子機構 Molecular mechanisms of cellular response to non-thermal atmospheric pressure plasma
抗酸化および抗炎症作用を有する化合物の探索 Exploratory study of anti-oxidative and anti-inflammatory compounds
最近の研究成果 Research Results
Takemoto R., Kamiya T., Atobe T., Hara H., Adachi T., Regulation of lysyl oxidase expression in THP-1 cellderived M2-like macrophages, J Cell Biochem 122, 777-786 (2021).
Kondo M., Hara H., Kamijo F., Kamiya T., Adachi T., 6-Hydroxydopamine disrupts cellular copper homeostasis in human neuroblastoma SH-SY5Y cells, Metallomics 13, mfab041 (2021).
