Differential effect of radiation on endothelial cell function in rectal cancer and normal rectum

Hirudin ameliorates intestinal radiation toxicity in the rat: support for thrombin inhibition as strategy to minimize side‐effects after radiation therapy and as countermeasure against radiation exposure

“…Our findings agree with van der Meeren et al, who found increased TF mRNA in mouse lung 10-18 days after irradiation [18]. The present study also complements previous studies from our laboratory, demonstrating deficient expression of endothelial thrombomodulin and increased expression of PAR1 in irradiated bowel both in the acute phase and the chronic phase of radiation enteropathy in irradiated animals, as well as in patients who have received radiation therapy [2,19,20]. Increased VWF immunoreactivity is a late phenomenon in irradiated kidney in vivo, but we have not observed consistent increase in VWF in irradiated intestine [19].…”

uPA and PAI-1 in Rectal Cancer—Relationship to Radiotherapy and Clinical Outcome

“…We cannot confirm these results, as we found no difference between irradiated and nonirradiated tumor tissue. Richter et al stipulated that lower levels of uPA would mirror a reduced invasive capacity in tumor cells caused by radiotherapy [28], but we found no correlations between uPA levels and tumor characteristics or cancer related outcome.…”

“…We believe that the activation of uPA in rectal mucosa is part of the inflammatory response to radiotherapy. In tumor tissue, Richter et al found a lower levels of uPA in irradiated tumor cells [28]. We cannot confirm these results, as we found no difference between irradiated and nonirradiated tumor tissue.…”

Simvastatin Ameliorates Radiation Enteropathy Development After Localized, Fractionated Irradiation by a Protein C-Independent Mechanism

“…In the acute phase, radiation increases endothelial cell permeability and expression of chemokines and adhesion molecules, and causes loss of vascular thromboresistance (3,4). Radiation-induced loss of vascular thromboresistance is a result of decreased fibrinolytic activity (24), increased expression of tissue factor (TF) (25,26) and von Willebrand factor (27), and decreased expression of prostacyclin (28) and TM (5,(29)(30)(31). TM is a transmembrane glycoprotein, located on the luminal surface of endothelial cells in most normal blood vessels.…”