This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Ito, S. Articles by Wilson, S. E. Search for Related Content PubMed PubMed Citation Articles by Ito, S. Articles by Wilson, S. E. Social Bookmarking                         What's this?

Effect of Coacervated -Elastin on Proliferation of Vascular Smooth Muscle and Endothelial Cells

Second Department of Surgery, Tokyo Medical College, Tokyo, Japan.

Shin Ishimaru, MD

Second Department of Surgery, Tokyo Medical College, Tokyo, Japan.

Samuel E. Wilson, MD

Department of Surgery, University of California, Irvine, California.

The arterial wall injury associated with arterial graft implantation causes smooth muscle cells (SMCs) in the media to migrate and proliferate in the intima at the graft-artery junction resulting in anastomotic intimal hyperplasia (AIH). An important step in devel oping a small-diameter prosthesis may be to stimulate endothelialization and thereby inhibit AIH. In this study, we investigated the effect of coacervated and crosslinked -elastin on proliferation of SMCs and endothelial cells (ECs) in vitro. Coacervation is an important step in the conversion of proelastin to make an elastin fiber in vivo.

SMCs and ECs were prepared from porcine aortic media and endothelium, respec tively. SMCs and ECs (three to five passages, 4 x 10 ⁴ cells/well) were seeded onto 12 well plates, coated and crosslinked with 0 or 10 mg/mL of coacervated -elastin. After the 1st, 2nd, or 3rd day of cultivation, proliferation was assayed by scintillation counting of [³H]-thymidine incorporation. For the 4th day only, 0, 0.1, 1, 10 mg/mL concentration of coacervated -elastin was coated and crosslinked. (continued on next page) SMC proliferation (1st, 2nd day: p<0.005; 3rd, 4th day: p<0.0001) was significantly inhibited over time and dose dependently, eg, 0.1 mg/mL (45.7 ±2.3%: % of control p<0.005), 1 mg/mL (5.9 ±0.7%, p<0.0005), 10 mg/mL (2.8 ±0.4%, p<0.0005). EC proliferation was inhibited over time by 10 mg/mL of coacervated -elastin (2nd, 3rd day: p<0.005; 4th day: p<0.0001), but proliferation (132.8 ±9.9%: % of control p=NS) was stimulated by 0.1 mg/mL of coacervated -elastin.

These results suggest that coating and crosslinking a coacervated -elastin into the structure of arterial prosthesis may inhibit AIH and stimulate endothelialization.

Angiology, Vol. 49, No. 4, 289-297 (1998)
DOI: 10.1177/000331979804900407


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?