Literature DB >> 7486232

Migration behavior of human smooth muscle cells cultivated from restenotic and primary lesions.

R Brandl1, P C Maurer, B Höfling, G Bauriedel.   

Abstract

Subintimal smooth muscle cell (SMC) migration is considered an essential determinant of arteriosclerosis and neointimal formation. In this study, a cell culture model was established to characterize migration activity of SMCs originating from restenotic and primary lesions. Plaques from symptomatic stenoses of 32 patients (19 men, 13 women; 4 carotid, 17 peripheral, 11 coronary lesions) were removed by percutaneous atherectomy or direct operative approach. Ten patients suffered from recurrent stenosis. Cell cultures were established by explantation of tissue samples. By indirect immunofluorescence microscopy, SMCs were shown to be the predominant cell type of all advanced lesions irrespective of their origin. The spontaneous cellular motility of SMCs was analyzed in vitro by means of a computer-assisted observation system. Cells of all groups exhibited random motility. SMC migratory velocity was found to be significantly (P < 0.001) greater in cells from restenotic lesions than in those from primary plaques. In conclusion, migration behavior of human SMCs originating from arteriosclerotic lesions may be quantified in vitro as a functional determinant characterizing restenotic versus primary lesions.

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Year:  1995        PMID: 7486232     DOI: 10.1177/000331979504601101

Source DB:  PubMed          Journal:  Angiology        ISSN: 0003-3197            Impact factor:   3.619


  1 in total

1.  Novel small leucine-rich repeat protein podocan is a negative regulator of migration and proliferation of smooth muscle cells, modulates neointima formation, and is expressed in human atheroma.

Authors:  Randolph Hutter; Li Huang; Walter S Speidl; Chiara Giannarelli; Paul Trubin; Gerhard Bauriedel; Mary E Klotman; Valentin Fuster; Juan J Badimon; Paul E Klotman
Journal:  Circulation       Date:  2013-09-16       Impact factor: 29.690

  1 in total

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