title: Coxsackievirus B3-induced apoptosis and caspase-3.
abstract: Cell death can be classified into two categories: apoptosis and necrosis. Apoptotic pathway can be either caspase-dependent or caspase-independent. Caspase-independent cytopathic effect (CPE) has been described. In order to evaluate the pattern of HeLa cell death induced by Coxsackievirus B3 (CVB3) and whether apoptosis involves caspase activation, we co-cultivated HeLa cells with CVB3 and detected the cytopathic changes, the alteration of mRNA and protein expression of caspase-3 gene plus caspase-3 activity, as well as analyzing DNA fragmentation before and after caspase-3 activity inhibition. According to the results, we propose that CVB3 may induce apoptosis and necrosis in HeLa cells, the latter appearing much earlier. Caspase-3 is activated at the levels of both transcription and translation, and procaspase-3 is proteolytically cleaved, thus leading to the continuous increasing of both caspase-3 precursor protein and its subunit. However, besides CPE, apoptosis induced by CVB3 is not a direct consequence of the activation of caspase-3, or caspase-3 is not the only effector molecule in apoptotic cell death, for caspase-3 inhibitor can not decrease DNA fragmentation. Some other biochemical mechanisms may participate in the process, whose role weakens the effect of inhibiting caspase-3 activity.
authors.affiliation: Department of Microbiology and Parasitology, Shanghai Second Medical University, Shanghai 200025, China.
authors.forename: Jian Ping
authors.initials: JP
authors.lastname: Yuan
authors.forename: Wei
authors.initials: W
authors.lastname: Zhao
authors.forename: Hong Tao
authors.initials: HT
authors.lastname: Wang
authors.forename: Kai Yu
authors.initials: KY
authors.lastname: Wu
authors.forename: Tao
authors.initials: T
authors.lastname: Li
authors.forename: Xiao Kui
authors.initials: XK
authors.lastname: Guo
authors.forename: Shan Qing
authors.initials: SQ
authors.lastname: Tong
mesh_terms: D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D053148:Caspase 3; D061945:Caspase Inhibitors; D020169:Caspases / Q000235:genetics / Q000378:metabolism*; D053938:DNA Fragmentation / Q000187:drug effects; D029822:Enterovirus B, Human / Q000502:physiology*; D004789:Enzyme Activation / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005434:Flow Cytometry; D006367:HeLa Cells / Q000648:ultrastructure / Q000821:virology; D006801:Humans; D008854:Microscopy, Electron; D009842:Oligopeptides / Q000494:pharmacology; D014176:Protein Biosynthesis / Q000235:genetics; D012333:RNA, Messenger / Q000378:metabolism; D013997:Time Factors; D014158:Transcription, Genetic / Q000235:genetics
chemical_list: D061945:Caspase Inhibitors; D004791:Enzyme Inhibitors; D009842:Oligopeptides; D012333:RNA, Messenger; C505407:CASP3 protein, human; D053148:Caspase 3; D020169:Caspases