Inhibition of endothelial regeneration by type-beta transforming growth factor from platelets.
Damage to the vessel wall is a signal for endothelial migration and replication and for platelet release at the site of injury. Addition of transforming growth factor-beta (TGF-beta) purified from platelets to growing aortic endothelial cells inhibited [3H]thymidine incorporation in a concentration-dependent manner. A transient inhibition of DNA synthesis was also observed in response to wounding; cell migration and replication are inhibited during the first 24 hours after wounding. By 48 hours after wounding both TGF-beta-treated and -untreated cultures showed similar responses. Flow microfluorimetric analysis of cell cycle distribution indicated that after 24 hours of exposure to TGF-beta the cells were blocked from entering S phase, and the fraction of cells in G1 was increased. The inhibition of the initiation of regeneration by TGF-beta could allow time for recruitment of smooth muscle cells into the site of injury by other platelet components.
Heimark
R L
RL
Twardzik
D R
DR
Schwartz
S M
SM
D000818:Animals; D001792:Blood Platelets / Q000502:physiology*; D002453:Cell Cycle / Q000187:drug effects; D002465:Cell Movement / Q000187:drug effects; D002478:Cells, Cultured; D004727:Endothelium / Q000166:cytology / Q000502:physiology*; D005434:Flow Cytometry; D006131:Growth Inhibitors; D006801:Humans; D066298:In Vitro Techniques; D010455:Peptides / Q000494:pharmacology*; D051381:Rats; D012038:Regeneration; D015291:Transforming Growth Factors
D006131:Growth Inhibitors; D010455:Peptides; D015291:Transforming Growth Factors