title: Reactive oxygen species induce cell death via Akt signaling in rat osteoblast-like cell line ROS 17/2.8.
abstract: In bones, osteoblasts are responsible for bone formation. The cell death of osteoblasts may cause a series of bone diseases and lead to bone loss, such as osteoarthrosis, hyperparathyroidism, and Paget's disease. Reactive oxygen species (ROS) are reported as a main factor for osteoblast cell death and further several bone diseases. However, the detailed mechanism is still largely unknown. Here, we found that ROS could induce cell death of rat osteoblast-like cell line ROS 17/2.8 via Akt (protein kinase B). Also, the mammalian target of rapamycin signaling was involved in this process. Our findings could help to reveal the cellular mechanism of osteoblast cell death, which is served for the pursuit of clinical treatment targets of relative bone diseases.
authors.affiliation: Department of Orthopedics, Chengdu Military General Hospital, Jinniu District, Chengdu, China zhangbo0320@yahoo.com.
authors.forename: Bo
authors.initials: B
authors.lastname: Zhang
authors.affiliation: Department of Orthopedics, Chengdu Military General Hospital, Jinniu District, Chengdu, China.
authors.forename: Qing-yun
authors.initials: QY
authors.lastname: Xie
authors.affiliation: Department of Orthopedics, Chengdu Military General Hospital, Jinniu District, Chengdu, China.
authors.forename: Yi
authors.initials: Y
authors.lastname: Quan
authors.affiliation: Department of Orthopedics, Chengdu Military General Hospital, Jinniu District, Chengdu, China.
authors.forename: Xian-ming
authors.initials: XM
authors.lastname: Pan
authors.affiliation: Department of Orthopedics, Chengdu Military General Hospital, Jinniu District, Chengdu, China.
authors.forename: Dong-fa
authors.initials: DF
authors.lastname: Liao
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D015415:Biomarkers / Q000378:metabolism; D001862:Bone Resorption / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D002460:Cell Line; D015536:Down-Regulation / Q000187:drug effects; D006861:Hydrogen Peroxide / Q000633:toxicity; D007700:Kinetics; D010006:Osteoblasts / Q000166:cytology / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D016877:Oxidants / Q000633:toxicity; D018384:Oxidative Stress / Q000187:drug effects; D010766:Phosphorylation / Q000187:drug effects; D011499:Protein Processing, Post-Translational / Q000187:drug effects; D051057:Proto-Oncogene Proteins c-akt / Q000037:antagonists & inhibitors* / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects; D058570:TOR Serine-Threonine Kinases / Q000037:antagonists & inhibitors* / Q000737:chemistry / Q000378:metabolism; D051025:bcl-Associated Death Protein / Q000378:metabolism
chemical_list: C494821:Bad protein, rat; D015415:Biomarkers; D016877:Oxidants; D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D051025:bcl-Associated Death Protein; D006861:Hydrogen Peroxide; C546845:mTOR protein, rat; C494920:Akt1 protein, rat; D051057:Proto-Oncogene Proteins c-akt; D058570:TOR Serine-Threonine Kinases
keywords: Akt; ROS 17/2.8; cell death; mTOR signaling; reactive oxygen species