title: Sequential induction of Hsp25 and proliferating cell nuclear antigen in the kidney after burn.
abstract: Burn injury elicits a wide range of intracellular signaling events leading to alterations in phenotypes of distant organs. Renal dysfunction is one of several serious postburn complications. To better understand the underlying mechanisms of renal dysfunction among burn patients, we investigated alterations in the expression of heat shock proteins (Hsps) and cell cycle-associated proteins in the kidney after burn. Following an approximately 18% total body surface area burn, blood and kidney samples were harvested from mice at several time points. Serum levels of blood urea nitrogen increased significantly at 3 h and returned to basal levels at Day 1 implying a transient dysfunction of glomerular filtration. The expression of Hsp25 was increased at Day 1, whereas no changes in Hsp70 expression were observed. An increase in proliferating cell nuclear antigen (PCNA), a marker of cell proliferation, peaked at Day 3, and its expression was predominantly limited to cells appearing to be tubular epithelial cells in the cortex. In contrast, no significant alterations in the p21 mitosis inhibitor were noted. Furthermore, increases in histones H1 and H2A at Day 3 paralleled the PCNA induction suggesting a burn-mediated alteration in cell cycle activities. The results from this study suggest that a sizeable burn may trigger sequential activation of signaling events involved in the early pathogenesis and subsequent recovery of the kidney after burn.
authors.affiliation: Burn Research, Shriners Hospitals for Children Northern California and Department of Surgery, University of California at Davis, Sacramento, CA 95817, USA.
authors.forename: Jayoung
authors.initials: J
authors.lastname: Jeong
authors.forename: David G
authors.initials: DG
authors.lastname: Greenhalgh
authors.forename: Kiho
authors.initials: K
authors.lastname: Cho
mesh_terms: D000818:Animals; D001806:Blood Urea Nitrogen; D015153:Blotting, Western; D002056:Burns / Q000097:blood / Q000378:metabolism* / Q000473:pathology; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins / Q000096:biosynthesis / Q000235:genetics; D004195:Disease Models, Animal; D005260:Female; D005786:Gene Expression Regulation; D018840:HSP70 Heat-Shock Proteins / Q000096:biosynthesis; D006360:Heat-Shock Proteins / Q000096:biosynthesis* / Q000235:genetics; D006657:Histones / Q000378:metabolism; D007124:Immunoenzyme Techniques; D007668:Kidney / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D018832:Molecular Chaperones; D009363:Neoplasm Proteins / Q000096:biosynthesis* / Q000235:genetics; D018809:Proliferating Cell Nuclear Antigen / Q000096:biosynthesis*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: C493957:Cdkn1a protein, mouse; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D018840:HSP70 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D006657:Histones; C486113:Hsbp1 protein, mouse; D018832:Molecular Chaperones; D009363:Neoplasm Proteins; D018809:Proliferating Cell Nuclear Antigen; D012333:RNA, Messenger