Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1997-1-10
pubmed:abstractText
The purpose of the present study was to determine whether heat shock pretreatment would protect pulmonary endothelial cells and alveolar macrophages against hydrogen peroxide (H2O2)-induced injury. The bovine pulmonary artery endothelial cells (BPAECs) heat-shocked (42 degrees C for 2 h) prior to exposure to H2O2 (1 mmol/L for 45 min) showed significant decrease in H2O2-mediated increment of release of lactate dehydrogenase and production of thiobarbituric acid-reactive substances, and obvious alleviation in H2O2-induced decrease in activities of catalase and superoxide dismutase. Heat-shocked (42 degrees C for 2 h) rat pulmonary alveolar macrophages (PAMs) also obtained acquired resistance to injury by subsequent exposure of 1, 2, or 3 mmol/L H2O2 for 45 min. Simultaneously with this acquired oxidative resistance, Northern blot analysis showed that heat-shocked BPAECs and PAMs, contained an increased level of mRNA coding for the inducible form of heat shock protein 70 (HSP70), and Western blot analysis indicated that there were increased expression of HSP70. Inhibition of protein synthesis by cycloheximide (25 micrograms/mL) and inhibition of RNA synthesis by actinomycin D (5 micrograms/mL) prevented the cytoprotection against H2O2. These results are consistent with the hypothesis that heat shock pretreatment would protect pulmonary endothelial cells and alveolar macrophages against H2O2-induced injury, and possibly that HSPs play a role in this cytoprotection.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1073-2322
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
134-41
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:8856848-Animals, pubmed-meshheading:8856848-Cattle, pubmed-meshheading:8856848-Cells, Cultured, pubmed-meshheading:8856848-Cycloheximide, pubmed-meshheading:8856848-Dactinomycin, pubmed-meshheading:8856848-Endothelium, Vascular, pubmed-meshheading:8856848-Gene Expression Regulation, pubmed-meshheading:8856848-HSP70 Heat-Shock Proteins, pubmed-meshheading:8856848-Heat-Shock Proteins, pubmed-meshheading:8856848-Hot Temperature, pubmed-meshheading:8856848-Hydrogen Peroxide, pubmed-meshheading:8856848-Macrophages, Alveolar, pubmed-meshheading:8856848-Molecular Weight, pubmed-meshheading:8856848-Nucleic Acid Synthesis Inhibitors, pubmed-meshheading:8856848-Protein Synthesis Inhibitors, pubmed-meshheading:8856848-Pulmonary Artery, pubmed-meshheading:8856848-RNA, Messenger, pubmed-meshheading:8856848-Rats
pubmed:year
1996
pubmed:articleTitle
Heat shock pretreatment prevents hydrogen peroxide injury of pulmonary endothelial cells and macrophages in culture.
pubmed:affiliation
Department of Pathophysiology, Hunan Medical University, Changsha, People's Republic of China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't