Biochemistry of Ischemic Reperfusion Injury
Abstract
Dermal microvascular endothelial cells when exposed to hypoxic conditions show a rapid induction of several proteins that do not increase in other cell types exposed to the same conditions of hypoxia. These new proteins differ from stress proteins, are induced rapidly, and are expressed transiently. They include a group of acidic proteins with molecular weights in the range of 100120,000 and a least one glycoprotein. This response is accompanied by a transient overall increase in protein synthesis as determined by the incorporation of radio labeled methionine. The changes seen in proteins synthesized by dermal microvascular endothelial cells takes place in the same time scale as ischemia-reperfusion injury and may reflect the specialized change of functions of the microvasculature observed under conditions of hypoxic stress in vivo. Since inflammation following ischemia is responsible for the subsequent tissue pathology, the sequential changes in the expression of four protooncogenes, c-fos, c-myc, c-sis and H-ras were determined following activation with the inflammatory mediator phorbol myristate acetate. Differences in the extent of activation and kinetics of each oncogene were determined. Phorbol myristate acetate activates protein kinase C, and suggests a close link between activation of protein phosphorylation, regulation in the synthesis of c- myc, c-sis, and c-fos mRNA and changes in the morphology and inflammatory response of dermal microvascular endothelial cells.
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 21, 1993
- Accession Number
- ADA271773
Entities
People
- Marvin A. Karasek
Organizations
- Stanford University