Studies on neovascularization during GVHD
| Model/observation . | References . |
|---|---|
| Animal | |
| Local GVH reactions occur after injection of allogeneic lymphocytes. | 20,,–23 |
| When immunocompetent splenocytes are injected intracutaneously into histoincompatible hosts, neovascularization occurs. There is a positive correlation between the number of injected cells and the degree of neovascularization. | 24 |
| GVHD is associated with neovascularization in target organs. | 25 |
| In irradiated hosts with GVHD neovascularization is due to vasculogenesis that is mediated by donor-derived endothelial progenitor cells. | 25 |
| The inhibition of neovascularization with monoclonal antibodies against monomers of vascular endothelial cadherin ameliorates GVHD. | 25 |
| Anti-VEGFR1/anti-VEGFR2 antibodies after allo-BM transplantation inhibit hematopoietic reconstitution. | 25 |
| Human | |
| Circulating endothelial cells are increased in HSC transplant recipients. Only donor-derived circulating endothelial cells have a high capacity to proliferate. | 36 |
| Donor BM-derived vasculogenesis contributes to neovascularization in the skin during GVHD. | 37,–39 |
| Donor BM-derived vasculogenesis contributes to neovascularization in the intestines during GVHD. | 37 |
| Donor-derived endothelial cells are more numerous and preferentially distributed in the areas of severe acute GVHD damage. | 38 |
| In gastric biopsies the vascular density is greater in patients with acute GVHD than in healthy controls. | 34 |
| In skin biopsies from patients with acute GVHD, there are areas with high vascular density. | 35 |
| There is a positive correlation between a low VEGF serum level and the occurrence of GVHD. | 40 |
| Single nucleotide polymorphisms leading to low VEGF production are associated with a higher incidence of GVHD. | 41 |
| High VEGF serum levels after HSCT are associated with less severe GVHD (there was a trend; however, the association was statistically not significant). | 42 |
| Treatment with bevacizumab (anti–VEGF-A mAb) before autologous HSCT has no major negative effect on hematopoietic reconstitution. | 43 |
| Model/observation . | References . |
|---|---|
| Animal | |
| Local GVH reactions occur after injection of allogeneic lymphocytes. | 20,,–23 |
| When immunocompetent splenocytes are injected intracutaneously into histoincompatible hosts, neovascularization occurs. There is a positive correlation between the number of injected cells and the degree of neovascularization. | 24 |
| GVHD is associated with neovascularization in target organs. | 25 |
| In irradiated hosts with GVHD neovascularization is due to vasculogenesis that is mediated by donor-derived endothelial progenitor cells. | 25 |
| The inhibition of neovascularization with monoclonal antibodies against monomers of vascular endothelial cadherin ameliorates GVHD. | 25 |
| Anti-VEGFR1/anti-VEGFR2 antibodies after allo-BM transplantation inhibit hematopoietic reconstitution. | 25 |
| Human | |
| Circulating endothelial cells are increased in HSC transplant recipients. Only donor-derived circulating endothelial cells have a high capacity to proliferate. | 36 |
| Donor BM-derived vasculogenesis contributes to neovascularization in the skin during GVHD. | 37,–39 |
| Donor BM-derived vasculogenesis contributes to neovascularization in the intestines during GVHD. | 37 |
| Donor-derived endothelial cells are more numerous and preferentially distributed in the areas of severe acute GVHD damage. | 38 |
| In gastric biopsies the vascular density is greater in patients with acute GVHD than in healthy controls. | 34 |
| In skin biopsies from patients with acute GVHD, there are areas with high vascular density. | 35 |
| There is a positive correlation between a low VEGF serum level and the occurrence of GVHD. | 40 |
| Single nucleotide polymorphisms leading to low VEGF production are associated with a higher incidence of GVHD. | 41 |
| High VEGF serum levels after HSCT are associated with less severe GVHD (there was a trend; however, the association was statistically not significant). | 42 |
| Treatment with bevacizumab (anti–VEGF-A mAb) before autologous HSCT has no major negative effect on hematopoietic reconstitution. | 43 |