Cyclosporin A inhibits smooth muscle proliferation in the vascular response to injury.
AUTOR(ES)
Jonasson, L
RESUMO
The arterial response to injury is dominated by proliferation of smooth muscle cells and infiltration of blood-borne cells in the vascular intima. Arterial smooth muscle cell proliferation is under growth factor control, but how this regulation operates in vivo is unclear. We studied the effect on arterial response to mechanical injury of cyclosporin A, a drug that inhibits T-lymphocyte activation. Cyclosporin A treatment at surgery caused a persistent inhibition of the intimal proliferative lesion. Cyclosporin A also inhibited expression of Ia antigens on smooth muscle cells in situ but had no direct effects on smooth muscle cell proliferation in culture. Therefore, the inhibition of intimal cell proliferation appears to be mediated via the immune system.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=279979Documentos Relacionados
- Carvedilol, a cardiovascular drug, prevents vascular smooth muscle cell proliferation, migration, and neointimal formation following vascular injury.
- Fibroblast growth factor stimulates angiotensin converting enzyme expression in vascular smooth muscle cells. Possible mediator of the response to vascular injury.
- Role of CD44 in the reaction of vascular smooth muscle cells to arterial wall injury.
- Role of CD44 in the reaction of vascular smooth muscle cells to arterial wall injury.
- T lymphocytes inhibit the vascular response to injury.
