The blood vessel wall responds to injury by proliferation of its cellular elements in the intima. This intimal proliferation is a common cause of failure in clinical vascular reconstruction, and may be partly mediated by local antoregulatory interactions between the cellular elements in the vascular wall. It is the overall objective of this project to define the nature of vascular cell interactions with special reference to the development of intimal hyperplasia. Using human endothelial and vascular smooth muscle (VSM) cells in single cell coculture systems the mutual ability of these cells to modulate their respective proliferation, migration, and secretion will be investigated. Uptake of H3 thymidine and in vitro attachment and migration assays will be used in these studies. In a rat model of vascular grafting, the relationship of endothelial healing to VSM cell proliferation and intimal hyperplasia will be investigated using light and electron microscopy, planimetry, and thymidine autoradiography. Data from these studies will provide a basis for the development of specific intervention to prevent intimal hyperplasia, thereby improving the results of vascular reconstruction.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
First Independent Research Support & Transition (FIRST) Awards (R29)
Project #
1R29HL039622-01
Application #
3471677
Study Section
Surgery, Anesthesiology and Trauma Study Section (SAT)
Project Start
1988-03-01
Project End
1993-02-28
Budget Start
1988-03-01
Budget End
1989-02-28
Support Year
1
Fiscal Year
1988
Total Cost
Indirect Cost
Name
Massachusetts General Hospital
Department
Type
DUNS #
City
Boston
State
MA
Country
United States
Zip Code
02199