Heparin inhibits human coronary artery smooth muscle cell migration

Kohno, Masakazu; Yokokawa, Koji; Yasunari, Kenichi; Minami, Mieko; Kano, Hiroaki; Mandal, Anil K.; Yoshikawa, Junichi

« Previous Next »Metabolism - Clinical and Experimental
Volume 47, Issue 9 , Pages 1065-1069, September 1998

Heparin inhibits human coronary artery smooth muscle cell migration☆

Masakazu Kohno
- Address reprint requests to Masakazu Kohno, MD, The First Department of Internal Medicine, Osaka City University Medical School, 1-5-7 Asahi-machi, Abeno-ku, Osaka 545, Japan.
- First Department of Internal Medicine, Osaka City University Medical School, Osaka, Japan
- Department of Medicine, Wright State University, Dayton, OH, USA
Koji Yokokawa
- First Department of Internal Medicine, Osaka City University Medical School, Osaka, Japan
- Department of Medicine, Wright State University, Dayton, OH, USA
Kenichi Yasunari
- First Department of Internal Medicine, Osaka City University Medical School, Osaka, Japan
- Department of Medicine, Wright State University, Dayton, OH, USA
Mieko Minami
- First Department of Internal Medicine, Osaka City University Medical School, Osaka, Japan
- Department of Medicine, Wright State University, Dayton, OH, USA
Hiroaki Kano
- First Department of Internal Medicine, Osaka City University Medical School, Osaka, Japan
- Department of Medicine, Wright State University, Dayton, OH, USA
Anil K. Mandal
- First Department of Internal Medicine, Osaka City University Medical School, Osaka, Japan
- Department of Medicine, Wright State University, Dayton, OH, USA
Junichi Yoshikawa
- First Department of Internal Medicine, Osaka City University Medical School, Osaka, Japan
- Department of Medicine, Wright State University, Dayton, OH, USA

Received 20 July 1997; accepted 30 March 1998.

Abstract

Heparin, an anticoagulant, has been shown to reduce neointimal proliferation and restenosis following vascular injury in experimental studies, but the clinical trials of heparin in coronary balloon angioplasty have been negative. The current study, therefore, examined the effect of heparin on basal or stimulated migration by serum and platelet-derived growth factor (PDGF)-BB in cultured human coronary artery smooth muscle cells (SMCs) by Boyden's chamber method. In addition, the reversibility of the heparin effect on human coronary artery SMC migration was examined. Fetal calf serum (FCS) and PDGF-BB stimulated SMC migration in a concentration-dependent manner. Heparin in moderate to high concentration (10 to 100 U/mL) exhibited concentration-related inhibition of FCS- and PDGF-BB—stimulated SMC migration; however, a low concentration (1 U/mL) of heparin had no inhibitory effects. Heparin also had weak inhibitory effects on nonstimulated SMC migration. The SMCs that were exposed to a high concentration (100 U/mL) of heparin for 6 hours were capable of migrating after a short lag period of removal of heparin from the culture medium. These SMCs also showed recovery of responses to FCS and PDGF-BB by migrating significantly greater than the nonstimulated level. Furthermore, heparin-containing medium did not contain detached cells. These results indicate that heparin inhibits human coronary artery SMC migration, especially when stimulated by FCS or PDGF-BB, and that this inhibitory effect of hepari is reversible and not simply a function of killing cells.

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