Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Factors controlling smooth-muscle cell proliferation.

M A Reidy1

  • 1Department of Pathology, University of Washington, Seattle 98195.

Archives of Pathology & Laboratory Medicine
|December 1, 1992
PubMed
Summary

Basic fibroblast growth factor (bFGF) inhibits early smooth muscle cell replication after arterial injury. However, neither bFGF nor platelet-derived growth factor fully explains the development of intimal lesions.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Sphingosine 1-phosphate: a regulator of arterial lesions.

Arteriosclerosis, thrombosis, and vascular biology·2009
Same author

Modulation of smooth muscle proliferation in rat carotid artery by platelet-derived mediators and fibroblast growth factor-2.

Platelets·2001
Same author

Proliferation of intimal smooth muscle cells. Attenuation of basic fibroblast growth factor 2-stimulated proliferation is associated with increased expression of cell cycle inhibitors.

The Journal of biological chemistry·2001
Same author

Mitogen-activated protein kinases mediate matrix metalloproteinase-9 expression in vascular smooth muscle cells.

Arteriosclerosis, thrombosis, and vascular biology·2000
Same author

Phosphatidylinositol 3-kinase signaling is important for smooth muscle cell replication after arterial injury.

Arteriosclerosis, thrombosis, and vascular biology·2000
Same author

Cell signaling in injured rat arteries.

Thrombosis and haemostasis·1999

Area of Science:

  • Vascular biology
  • Cellular signaling
  • Arterial disease research

Background:

  • Arterial injury triggers smooth muscle cell (SMC) replication and intimal lesion formation.
  • Basic fibroblast growth factor (bFGF) and platelet-derived growth factor (PDGF) are implicated in SMC replication.

Purpose of the Study:

  • To investigate the roles of bFGF and PDGF in SMC replication and intimal lesion development after arterial injury.
  • To determine the efficacy of blocking antibodies against bFGF and PDGF in preventing these processes.

Main Methods:

  • Mechanical injury (balloon catheter) was induced in rat carotid arteries.
  • Infusion of blocking antibodies against bFGF and PDGF was administered.
  • SMC replication and intimal lesion development were assessed.

Main Results:

  • Antibodies to bFGF significantly inhibited early SMC replication post-injury.
  • Antibodies to bFGF did not inhibit intimal lesion development when administered at the time of injury.
  • PDGF was found to be crucial for SMC migration into the intima, not direct replication.
  • Neither antibody inhibited overall intimal SMC replication.

Conclusions:

  • bFGF plays a role in the initial smooth muscle cell replication following arterial injury.
  • PDGF is important for smooth muscle cell migration but not directly for replication.
  • The precise mechanisms driving intimal lesion proliferation remain incompletely understood.

Related Experiment Videos